Complaints, anamnesis, general inspection of patients with respiratory system pathology.
Physical methods of examination. Percussion and auscultation of lungs. Laboratory and instrumental methods of investigation in pulmonology.
Inquiry and general inspection of patients with diseases of digestive tract. Physical methods of examination of gastrointestinal tract. Palpation of an abdomen. Supplementary methods of gastrointestinal tract examination.
Main sybdromes in diseases of respiratory and digestive systems.
Examination of respiratory system
Complaints of patients with respiratory pathology
The main complaints typical for the respiratory system are dyspnoea, cough, bloody expectorations, and pain in the chest. Fever, asthenia, indisposition and loss of appetite are not infrequent.
Dyspnoea in its manifestation can be subjective, objective, or subjective and objective simultaneously. By subjective dyspnoea is understood the subjective feeling of difficult or laboured breathing. Objective dyspnoea is determined by objective examination and is characterized by changes in the respiration rate, depth, or rhythm, and also the duration of the inspiration or expiration. Diseases of the respiratory system are often accompanied by mixed (i.e. subjective and objective) dyspnoea. It is often associated with rapid breathing (tachypnoea). These symptoms occur in pneumonia, bronchogenic cancer, and in tuberculosis. Cases with purely subjective dyspnoea (in hysteria, thoracic radiculitis) or purely objective dyspnoea (in pulmonary emphysema or pleural obliteration) occur less frequently. Dyspnoea is possible with both normal and slow rate of breathing (bradypnoea). Three types of dyspnoea are differentiated by the prevalent breathing phase: inspiratory dyspnoea, expiratory dyspnoea and mixed dyspnoea when both expiration and inspiration become difficult.
Dyspnoea may be physiological (caused by heavy exercise) and pathological (associated with pathology of the respiratory organs, diseases of the cardiovascular and haemopoietic systems, and poisoning).
Dyspnoea associated with respiratory pathology may be of various aetiology. It can be caused by obstruction of the respiratory ducts, contraction of the respiratory surface of the lungs due to their compression by liquid or air accumulated in the pleural cavity, decreased pneumatization of the lung in pneumonia, atelectasis, infarction or decreased elasticity of the lungs. These conditions are associated with decreased total (vital) lung capacity and ventilation, which causes increased carbon dioxide content of blood, and acidosis of tissues due to accumulation in them of incompletely oxidized metabolites (lactic acid, etc.). The so-called alveolar-capillary block is also possible in some cases. This is associated with exudative and proliferative inflammation of the interstitial tissue in interstitial pneumonia or lung oedema.
A mechanical obstruction in the upper respiratory ducts (larynx, trachea) complicates and slows down passage of the air into the alveoli and causes inspiratory dyspnoea. When the trachea and a large bronchus are sharply contracted, both inspiration and expiration become difficult and noisy (stridulous respiration) occurs. Narrowed lumen in the fine bronchi and bronchioles due to inflammatory oedema and swelling of their mucosa, or else in spasms in the smooth muscles (bronchial asthma), interferes with normal air passage from the alveoli and the expiration becomes difficult. Expiratory dyspnoea thus develops. The patient has to assume a forced, sometimes sitting posture (orthopnoea) to remove the discomfort. Heavy dyspnoea, often followed by asphyxia, is called suffocation. It occurs also in acute oedema of the lungs, bronchiolitis in children, and in fibrinous bronchitis. Asphyxia arising as a sudden attack is asthma. Bronchial asthma, in which an attack of dyspnoea occurs as a result of spasms of smaller bronchi and is accompanied by difficult, lengthy and noisy expiration, is differentiated from cardiac asthma which is secondary to left heart failure and is often accompanied by lung oedema with very difficult expiration.
Cough is a complicated reflex act which is actually a defence reaction aimed at clearing the larynx, trachea, or bronchi from mucus or foreign material. An inflamed bronchial mucosa produces a secretion which acts on the sensitive reflexogenic zones in the respiratory mucosa to stimulate the nerve endings and to activate the coughing reflex.
Cough may be dry, without sputum, and moist which various amounts of sputum of different quality are expected. Some diseases are attended only by dry cough, e.g. laryngitis, dry pleurisy or compression of the main bronchi by the bifurcation lymph nodes (tuberculosis, lymphogranulomatosis, cancer metastases, etc.). Bronchitis, pulmonary tuberculosis, pneumosclerosis, abscess, or bronchogenic cancer of the lungs can be first attended by dry cough, which will then turn into moist one with expectoration of the sputum.
If a patient complains of cough with sputum, the physician should try to determine the amount of sputum expectorated during one fit and during the entire day; it is also important to know the time of the day during which the sputum is expectorated and the position of the body at which cough is provoked; the colour, odour, and other properties of sputum are also important. Morning cough is characteristic of patients with chronic bronchitis, bronchiectasis, lung abscess, and cavernous tuberculosis of the lungs. The sputum accumulates during the night sleep in the lungs and the bronchi, but as the patient gets up, the sputum moves to the neighbouring parts of the bronchi to stimulate the reflexogenic zones of the bronchial mucosa. This causes cough and expectoration of the sputum. The amount of the sputum expectorated during the morning may amount to two thirds of the entire daily expectoration. Depending on the gravity of the inflammatory process in patients with mentioned diseases, the daily amount of the expectorated sputum may vary from 10—15 ml to as much as 2 litres. In unilateral bronchiectasis, sputum may be better expectorated in a definite posture, for example, on the right side with bronchiectasis in the left lung, and vice versa. If bronchiectasis is found in the anterior region of the lungs, expectoration is easier in the supine position, and if in the posterior parts, in the prone position.
Many patients, particularly smokers, assume that coughing is a normal life experience. It may be difficult to quantify the problem, particularly if the cough is dry. If productive, work out the amount, an eggcupful a day perhaps? Is the sputum mucoid or purulent, is the sputum white or grey, or more yellow-green in colour?
Patients with pneumonia and bronchitis may complain of cough attacks during the entire day, but attacks may intensify by night (“evening” cough). “Night” cough is characteristic of tuberculosis, lymphogranulomatosis, or malignant newgrowths. Enlarged mediastinal lymph nodes in these diseases stimulate the reflexogenic zone of the bifurcation, especially during night when the tone of the vagus nerve increases, to produce the coughing reflex.
Cough is differentiated by its length. It may be permanent and periodic. Permanent cough is rarer and occurs in laryngitis, bronchitis, bronchogenic cancer of the lungs or metastases into the mediastinal lymph nodes, and in certain forms of pulmonary tuberculosis. Periodic cough occurs more frequently.
Cough is also classified by its loudness and timbre. Loud barking cough is characteristic of whooping cough, compressed trachea (due to retrosternal goitre or tumour), affection of the larynx and swelling of the false vocal cords, and in hysteria; soft cough or tussiculation (hacking cough) is characteristic of the first stage of acute lobar pneumonia, dry pleurisy and the early stage of pulmonary tuberculosis. Inflammation of the vocal cords is attended by strong cough while ulceration of the cords is characterized by voiceless cough.
Haemoptysis is expectoration of blood with sputum during cough. The physician must determine the origin of haemoptysis and the amount and character of blood expectorated with sputum. Haemoptysis can develop in diseases of the lungs and air ways (bronchi, trachea or larynx), as well as in diseases of the cardiovascular system. Pulmonary tuberculosis and cancer, virus pneumonia, bronchiectasis, abscess and gangrene of the lung, actinomycosis, tracheitis and laryngitis associated with virus influenza are often attended by haemoptysis. This symptom is also characteristic of some heart defects, thrombosis or embolism of the pulmonary arteries and subsequent pulmonary infarction.
If the patient has coughed up blood, find out whether this represents fine blood-streaking of the sputum or a more conspicuous amount. Is it a recent event, or has it happened periodically over several years? Did it follow a particularly violent bout of coughing?
The amount of blood expectorated with sputum is mostly scant. Blood appears in the form of thin streaks, or it may give diffuse colouration to the sputum, which can be jelly-like or foamy. Cavernous tuberculosis, bronchiectases, degrading tumour and pulmonary infarction may be attended by lung haemorrhage, which is usually accompanied with strong cough.
Blood expectorated with sputum can be fresh and scarlet, or altered. Scarlet blood in the sputum is characteristic of pulmonary tuberculosis, bronchogenic cancer, bronchiectasis, and actinomycosis of the lungs. Blood expectorated with sputum in acute lobar pneumonia (second stage) has the colour of rust (rusty sputum) due to decomposition of the red blood cells and formation of the pigment haemosiderin. Blood in the sputum is fresh and scarlet during the first 2-3 days in lung infarction while in subsequent 7-10 days it becomes altered.
Pain in the chest is classified by its location, origin, character, intensity, duration, and irradiation, by its connection with the respiratory movements, cough, and the posture. Pain may arise during the development of a pathological condition in the thoracic wall, the pleura, heart, and the aorta, and in diseases of the abdominal organs (by irradiation). Special clinical signs are characteristic of pain of any particular origin, and in this respect pain may have diagnostic value.
Pain in the chest in diseases of the respiratory organs depends on irritation of the pleura, especially of the costal and diaphragmal parts where sensitive nerve endings are found. (They are absent in the pulmonary tissue.) Pleura may be injured during its inflammation (dry pleurisy), in subpleural pneumonia (acute lobar pneumonia, lung abscess, pulmonary tuberculosis), in lung infarction, tumour metastasis into the pleura or development in it of the primary tumour, in injury (spontaneous pneumothorax, wound, rib fracture), in subdiaphragmal abscess, and in acute pancreatitis.
Localization of pain depends on the pathological focus. Pain in the left or right inferior part of the chest (pain in the side) is characteristic of dry pleurisy. Inflammation of the diaphragmal pleura may be manifested by pain in the abdomen to simulate acute cholecystitis, pancreatitis, or appendicitis.
Pleural pain is often piercing, while in diaphragmal pleurisy and spontaneous pneumothorax it is acute and intense. Pain is intensified in deep breathing, coughing, or when the patient lies on the healthy side. The respiration movements in this position become more intense in the affected side of the chest to strengthen friction of the inflamed pleura (rough from deposited fibrin). Pain lessens when the patient lies on the affected side. Pleural pain is also lessened when the chest is compressed to decrease the respiratory excursions.
Before concentrating on individual systems ask some general questions about the patient’s health. Is the patient sleeping well? If not, is there a problem getting to sleep or a tendency to wake in the middle of the night or in the early hours of the morning? Has there been weight loss, fevers, rashes or night sweats? This leads in to the systems’ enquiry. The questions surrounding the presenting complaint will often have completed the systematic enquiry for that organ and there is no need to repeat questions already asked but simply to indicate ‘see above’. Develop a routine that helps to avoid missing out a particular system.
Data of anamnesis
When questioning the patient the physician should determine the time the disease began. Acute onset is characteristic of acute pneumonia, especially acute lobar pneumonia. Pleurisy begins more gradually. A non-manifest onset and a prolonged course are characteristic of pulmonary tuberculosis and cancer. The onset of many diseases may be provoked by chills (bronchitis, pleurisy, pneumonia).
Determining epidemiological conditions is very important for establishing the cause of the disease. Thus influenzal pneumonia often occurs during epidemic outbreaks of influenza. Establishing contacts with tuberculosis patients is also very important. Specific features of the course of the disease and the therapy given (and its efficacy) should then be established.
When collecting the life anamnesis, the physician should pay attention to conditions under which the patient lives and works. Damp premises with inadequate ventilation or work in the open (builders, truck drivers, agricultural workers, etc.) can become the cause of acute inflammation of the lungs with more frequent conversion into chronic diseases. Some dusts are harmful and cause bronchial asthma. Coal dust causes a chronic disease of the lungs called anthracosis. Regular exposure to silica dust (cements, pottery, etc.) causes silicosis, the occupational fibrosis of the lungs.
The patient should give a detailed report of his past diseases of the lungs or pleura, which helps the physician establish connections between the present disease and diseases of the past history.
Data of objective examination
By inspection the examiner can reveal diffuse cyanosis in the case of respiratory failure:
Pay attention to colour of visible mucosa (cyanosis):
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Inspection of the neck shoves svelling of neck veins in elevation of intrathoracic pressure:
You can see swelling of neck veins in superior vena cava obstruction and dilation of superficial veins on the chest
Patients with chronic hypoxia develop clubbing fingers
Examination of the chest is done according to a definite plan. Inspection of a chest is divided on static and dynamic one.
Static inspection of the chest
The general configuration of the chest should first beestimated (position of the clavicles, supra- and subclavicular fossae, shoulder blades)$ the next step is to define the type, rrhythm and frequency of breathing, respiratory movements of the left and right shoulder blades, and of the shoulder girgle, and involvement of the accesory respiratory muscles in the breathing act. The patient should be better examined in the upright (standing or sitting) position with the chest being naked. Illumination of the body should be uniform.
Body symmetry is always an important notation during the inspection of the chest. Asymmetry in the chest may indicate serious underlying problems, such as pulmonary dysfunction. However, asymmetry is most often a sign of scoliosis, lateral curvature of the spine. Asymmetry requires further medical investigation.
The shape of the chest may be normal or pathological. A normal chest is characteristic of healthy persons with regular body built. Its right and left sides are symmetrical, the clavicles and the shoulder blades should be at one level and the supraclavicular fossae equally pronounced on both sides. Sinse all people with normal constitution are conventionally divided into three types, the chest has different shape in accordance with its constitutional type.
Pathological shape of the chest may be the result of congential bone defects and of vatious cjronic diseases (emphysema of the lungs, rickets, tuberculosis).
Normal form of the chest
. 1. Normosthenic (conical) chest in subjects with normosthenic constitution resembles a truncated cone whose bottom is formed by well-developed muscles of the shoulder girdle and is directed upward. The anteroposterior (sterno vertebral) diameter of the chest is smaller than the lateral (transverse) one, and the supraclavicular fossae are slightly pronounced. There is a distinct angle between the sternum and the manubrium (angulus Ludowici); the epigastric angle nears 90°. The ribs are moderately inclined as viewed from the side; the shoulder blades closely fit to the chest and are at the same level; the chest is about the same height as the abdominal part of the trunk.
2. Hypersthenic chest in persons with hypersthenic constitution has the shape of a cylinder. The anteroposterior diameter is about the same as the transverse one; the supraclavicular fossae are absent (level with the chest). The manubriosternal angle is indistinct; the epigastric angle exceeds 90°;
the ribs in the lateral parts of the chest are nearly horizontal, the intercostal space is narrow, the shoulder blades closely fit to the chest, the thoradc part of the trunk is smaller than the abdominal one.
3. Asthenic chest in persons with asthenic constitution is elongated, narrow (both the anteroposterior and transverse diameters are smaller thaormal); the chest is flat. The supra- and subclavicular fossae are distinctly pronounced. There is no angle between the sternum and the manubrium: the sternal bone and the manubrium make a straight “plate”. The epigastric angle is less than 90°. The ribs are more vertical at the sides, the tenth ribs are not attached to the costal arch (costa decima fluctuens); the intercostal spaces are wide, the shoulder blades are winged (separated from the chest), the muscles of the shoulder girdle are underdeveloped, the shoulders are sloping, the chest is longer than the abdominal part of the trunk.
Pathological chest
1. Emphysematous (barrel-like) chest resembles a hypersthenic chest in its shape, but differs from it by a barrel-like configuration, prominence of the chest wall, especially in the posterolateral regions, the intercostal spaces are enlarged. This type of chest is found in chronic emphysema of the lungs. Active participation of accessory respiratory muscles in the respiratory act (especially m. sternocleidomastoideus and m. trapezius), depression of the intercostal space, elevation of the entire chest during inspiration and relaxation of the respiratory muscles and lowering of the chest to the initial position during expiration become evident during examination of emphysema patients.
General appearance of a patient with pulmonary emphysema
2. Paralytic chest resembles the asthenic chest. It is found in emaciated patients, in general asthenia and constitutional underdevelopment; it often occurs in grave chronic diseases, more commonly in pulmonary tuberculosis and pneumosclerosis. During examination of patients with paralytic chest, marked atrophy of the chest muscles and asymmetry of the clavicles and dissimilar depression of the supraclavicular fossae can be observed along with typical signs of aslhenic chest. The shoulder blades are not at one level either, and their movements during breathing are asynchronous.
Paralytic chest
3. Rachitic chest (keeled or pigeon chest). It is characterized by a markedly greater anteroposterior diameter (compared with the transverse diameter) due to the prominence of the sternum (which resembles the keel of a boat.) The anterolateral surfaces of the chest are as if pressed on both sides and therefore the ribs meet at an acute angle at the sternal bone, while the costal cartilages thicken like beads at points of their transition to bones (rachitic beads). As a rule, these beads can be palpated after rickets only in children and youths.
1. Funnel chest has a funnel-shaped depression in the lower part of the sternum. This deformity can be regarded as a result of abnormal development of the sternum or prolonged compressing effect. In older times this chest would be found in shoemaker adolescents.
5. Foveated chest is almost the same as the funnel chest except that the depression is found mostly in the upper and the middle parts of the anterior surface of the chest. This abnormality occurs in syringomyelia, a rare disease of the spinal cord.
The chest may be abnormal in subjects with various deformities of the spine which arise as a result of injuries, tuberculosis of the spine, rheumatoid arthritis (Bekhterev’s disease), etc. Four types of spine deformities are distinguished: lateral curvature of the spine, called scoliosis; excessive forward and backward curvature of the spine (gibbus and kyphosis, respectively); forward curvature of the spine, generally in the lumbar region (lordosis); combination of the lateral and forward curvature of the spine (kyphoscoliosis).
Different types of chest deformities
The shape of the chest can readily change due to enlargement or diminution of one half of the chest (asymmetry of the chest). These changes can be transient or permanent.
The enlargement of the volume of one half of the chest can be due to escape of considerable amounts of fluid as the result of accumulation of fluid in the pleural cavity, or due to penetration of air inside the chest in injuries (pneumothorax). Levelling or protrusion of the intercostal spaces, asymmetry of the clavicles and the shoulder blades and also unilateral thoracic lagging can be observed during examination of the enlarged part of the chest.
One part of the chest may diminish due to pleural adhesion or complete closure of the pleural slit after resorption of effusion (after prolonged presence of the fluid in the pleural cavity); contraction of a considerable portion of the lung due to growth of connective tissue (pneumosclerosis) after acute or chronic inflammatory processes, such as acute lobar pneumonia (with subsequent carnification of the lung), lung infarction, pulmonary abscess, tuberculosis, etc.;resection of a pan or the entire lung; atelectasis (collapse of the lung or its portion) that may occur due to closure of the lumen in a large bronchus by a foreign body or a tumour growing into the lumen of the bronchus and causing its obturation. The closure of the air passage into the lung with subsequent resorption of air from the alveoli and a decrease in the volume of the lung diminish the corresponding half of the chest. The chest thus becomes asymmetrical, the shoulder of the affected side lowers, the clavicle and the scapula lower as well, and their movements during deep respiration become slower ttnd limited; the supra- and subclavicular fossae become more depressed, the intercostal spaces decrease in size or become invisible. The marked depression of the supraclavicular fossa on one side often depends on the diminution of the apex of a fibrosis-affected lung.
Dynamic inspection. Inspection of the lungs involves primarily observation of respiratory movements, which are discussed. Respirations are evaluated for (1) rate (number per minute), (2) rhythm (regular, irregular, or periodic), (3) depth (deep or shallow), and (4) quality (effortless, automatic, difficult, or labored). The doctor also notes the character of breath sounds based on inspection without the aid of auscultation, such as noisy, grunting, snoring, or heavy.
Movement of the chest wall is noted. It should be symmetric bilaterally and coordinated with breathing. During inspiration the chest rises and expands, the diaphragm descends, and the costal angle increases. During expiration the chest falls and decreases in size, the diaphragm rises, and the costal angle narrows.
Any asymmetry of movement is an important pathologic sign and is reported. Decreased movement on one side of the chest may indicate pneumonia, pneumothorax, atelectasis, or an obstructive foreign body. Marked retraction of muscles either between the ribs (intercostal), above the sternum (suprasternal), or above the clavicles (supraclavicular) is always noted, because it is a sign of respiratory difficulty.
Normal respiratory rate is 16-20 per min. The respiratory rate is always evaluated in relation to general physical status. For example, tachypnea is expected with fever, because for every degree Fahrenheit elevation in temperature, the respiratory rate increases 4 breaths per minute. The usual ratio of breaths to heartbeats is 1:4.
Respiratory movements of the chest should be examined during inspection of the patient. In physiological conditions they are performed by the contraction of the main respiratory muscles: intercostal muscles, muscles of the diaphragm, and partly the abdominal wall muscles. The so-called accessory respiratory muscles (mm. sternocleidomastoideus, trapezius, pectoralis major et minor, etc.) are actively involved in the respiratory movements in pathological conditions associated with difficult breathing.
The type, frequency, depth and rhythm of respiration can be determined by carefully observing the chest and the abdomen. Respiration can be costal (thoracic), abdominal, or mixed type.
Thoracic (costal) respiration. Respiratory movements are carried out mainly by the contraction of the intercostal muscles. The chest markedly broadens and slightly rises during inspiration, while during expiration it narrows and slightly lowers. This type of breathing is known as costal and is mostly characteristic of women.
Abdominal respiration. Breathing is mainly accomplished by the diaphragmatic muscles; during the inspiration phase the diaphragm contracts and lowers to increase rarefaction in the chest and to suck in air into the lungs. The intra-abdominal pressure increases accordingly to displace anteriorly the abdominal wall. During expiration the muscles are relaxed, the diaphragm rises, and the abdominal wall returns to the initial position. This type of respiration is also called diaphragmatic and is mostly characteristic of men.
Mixed respiration. The respiratory movements are carried out simultaneously by the diaphragv and the intercostals muscles.
Respiration rate may be determined by counting the movements of the chest or the abdominal wall, while the patient is being unware of the procedure (during examination of his pulse, for example). Iorm the respiration rate is within 16-20 breathing movements a min. It is increased in dyspnea and rises in the case of inhibition of respiratory center.
Causes of alteration of the respiratory rate:
1) narrowing of the lumen of small bronchi due to spasms or diffuse inflammation of their mucosa (bronchiolitis occurring mostly in children), which interfere with normal passage of air into the lungs;
2) decreased respiratory surface of the lungs due to their inflammation and tuberculosis, in collapse or atelectasis of the lung due to its compression (pleuricy with rffusion, hydrothorax, pneumothorax, mediastinal tumor), in obstruction or compression of the main bronchus by a tumor etc;
3) insufficient depth of breathing.
Pathological deceleration of respiration occurs in functional inhibition of the respiratory centre and its decreased excitability. It van be due to increased intracranial pressure in patients with cerebral tumor, meningitis, cerebral haemorrhage, or oedema of the brain, and also due to the toxic effect on the respiratory centre when toxic substahces are accumulated in the blood, e.g. in uraemia, hepatic or diabetic coma, and in certain acute infectious diseases.
Respiration depth. The depth of breathing is, determined by the volume of the inhaled and exhaled air at rest. This volume varies in an adult from 300 to 900 ml (500 ml on the average). Depending on depth, breathing can be either deep or superficial. Superficial (shallow) breathing often occurs in pathologically accelerated respiration when the length of the inspiration and the expiration phases becomes short. Deep breathing is, on the contrary, associated in most cases with pathological deceleration of the respiration rate. Deep and slow «respiration, with marked respiratory movements, is sometimes attended by noisy sounds. This is Kussmaul’s respiration. occurring in deep coma. In some pathological conditions, however, rare respiration can be shallow, while accelerated breathing deep. Rare superficial respiration can occur in sharp inhibition of the respiratory centre, pronounced lung emphysema, and sharp narrowing of the vocal slit or the trachea. Respiration becomes accelerated and deep in high fever and marked anaemia.
Respiration rhythm. Respiration of a healthy person is rhythmic, of uniform depth and equal length of the inspiration and expiration phases. Rhythm of the respiratory centre can be inhibited, in some types of oedema. Derangement of the respiratory function can (pause oedema in which a series of respiratory movements alternates with a pronounced (readily detectable) elongation of the respiratory pause (lasting from a few seconds to a minute) or to a temporary arrest of respiration (apnoea). This respiration is known as periodic.
Biot’s respiration is characterized by rhythmic but deep respiration movements which alternate (at approximately regular intervals) with 1ong respiratory pauses (from few seconds to half a minute). Biot’s respiration occurs in meningitis patients and in agony with disorders of cerebral circulation.
Cheyne-Stokes’ respiration is characterized by periods (from seconds to a minute) of cessation of respiration, followed by noiseless shallow respiration, which quickly deepens, becomes noisy to attain hj maximum at the 5-7th inhalation, and then gradually slows down to end with a new short respiratory pause. During such pauses, the patient often loses his sense of orientation in the surroundings or even faints, to recover from the unconscious condition after respiratory movements are restored. This respiratory disorder occurs in diseases causing acute or chronic insufficiency of cerebral circulation and brain hypoxia, and also in heavy poisoning. More frequently this condition develops during sleep and is more characteristic of aged persons with marked atherosclerosis of the cerebral arteries.
Undulant (wave-like) Grocco’s respiration somewhat resembles Cheyne-Stoke’s respiration exept that a weak shallow respiration occurs instead of the respiratory pause with subsequent deepening of the respiratory movement, followed by slowing down. This type of arrhythmic dyspnoea can probably be regarded as the early stages of the same pathological processes which are responsible for resembles Cheyne-Stoke’s respiration.
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Disorders of the respiratory rate Tachypnea is the increase of the respiratory rate. Bradypnea is the decrease of the respiratory rate. Dyspnea is the distress during breathing. Apnea is the cessation of breathing.
Disorders of the respiratory depth Hyperpnea is an increased depth. Hypoventilation is a decreased depth and irregular rhythm. Hyperventilation is an increased rate and depth.
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Pathological respiration
Pathological changes of rhythm and depth of respiration are as follows:
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The type of respiration disorder |
In which pathological conditions it takes place |
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1. |
Cheyne-Stoke’s respiration gradually increasing rate and depth with periods of apnea |
Acute and chronic insufficiency of cerebral circulation and brain hypoxia, heavy poisoning |
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2.
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Grocco’s respiration gradually increasing rate and depth without periods of apnea |
Early stages of the same pathological conditions as (1) |
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3. |
Biot’s respiration periods of hyperpnea alternating with apnea |
Meningitis, agony with disorders of cerebral circulation |
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4. |
Kussmaul’s respiration is hyperventilation, gasping and labored respiration, usually seen in diabetic coma or other states of respiratory acidosis |
Deep coma |
Palpation as a method of examination
Palpation involves the use of the doctor’s hands to feel texture, size, shape, consistency, and location of certain parts of the client’s body and also to identify areas the client reports as being tender or painful. This technique requires the doctor to move into the client’s personal space. It is important that the touch is gentle, hands are warm, and nails are short to prevent discomfort or injury to the client. Touch has cultural significance and symbolism. Each culture has its own understanding about the uses and meanings of touch. As a result, it is of utmost importance that doctors tell clients the purpose of their touch (e.g., “I’m feeling for lymph nodes now”) and manner and location of touch (e.g., “I’m going to press deeply on your abdomen to feel the organs”). Gloves are worn when palpating mucous membranes or any other area where contact with body fluids is possible.
The palmar surfaces of fingers and finger pads are more sensitive than the fingertips; thus they are better for determining position, texture, size, consistency, masses, fluid, and crepitus. The ulnar surface of the hand extending to the fifth finger is the most sensitive to vibration, whereas the dorsal surface of the hand is better for assessing temperature.
Palpation using the palmar surfaces of the fingers may be light or deep and is controlled by the amount of pressure applied. For example, when examining the abdomen, light palpation is accomplished by pressing to a depth of approximately 1 cm and is used to assess skin, pulsations, and tenderness. Deep palpation, accomplished by using one or both hands to press in up to 4 cm, is used to determine organ size and contour. Light palpation should always precede deep palpation because palpation may cause tenderness or disrupt fluid, which would interfere with collecting data by light palpation. A bimanual technique of palpation uses both hands, one anterior and one posterior, to entrap an organ or mass between the fingertips to assess size and shape. This technique is used to assess the kidneys and uterus.
The sequence and technique of palpation of a chest
Palpation of the chest in user for determination of following:
To locate the pain in the chest and its irradiation – carefully press with your fingers along each intercostal space.
Resistance or elasticity of the chest – is determined by exerting preassure of the examining hands from the front to the sides and on the back and the , sternum and also by palpation of intercostal spaces.
The strengs of voice conduction to the chest surface (vocal fremitus) – The palms of the hands are placed on the symmetrical parts of the chest and the patient is asked to utter loudly words with the letter “r” in them.
Palpation is used as an additional means of examination to verify findings of inspection (the shape of the chest, its dimensions, respiratory movements(, for determining local or profuse tenderness of the chest, its elasticity (resilience), vocal fremitus, pleural friction and sounds of fluid in the pleural cavity.
Palpation should be done by placing the palms on the symmetrical (left and right) parts of the chest. This examination helps follow the respiratory excursions and deviation of the chest movements from their normal course. During respiration the hands will move with the chest wall. The doctor evaluates the amount and speed of respiratory excursion, noting any asymmetry of movement. Normally the amplitude of movements are equal on both chest parts..
Evaluation of respiratory excursion
The epigastric angle as determined by palpation as well. The thumbs should be pressed tightly against the costal arch, their tips resting against the xiphoid process (ensiform cartilage).
Crepitation is felt as a coarse, cracking sensation as the hand presses over the affected area. It is the result of the escape of air from the lungs into the subcutaneous tissues from an injury or surgical intervention. Both pleural friction rubs and crepitation can usually be heard as well as felt.
Palpation is used to locate pain in the chest and its irradiation. For example, in rib fracture, pain is located over a limited site, namely at the point of the fracture. Displacement (careful!) of bone fractures will be attended in this case by a specific sound (crunch). Inflammation of the intercostal nerves and muscles also causes pain, but it can be felt during palpation over the entire intercostal space. Such pain is called superficial. It is intensified during deep breathing, when the patient bends to the affected side, or lies on this side.
Resilience or elasticity of the chest is determined by exerting pressure of the examining hands from the front to the sides of the chest or on the back at the sternum, and also by palpation of the intercostal spaces. The chest of a healthy person is elastic, plaint and yields under the pressure. In the presence of pleurisy with effusion, or pleural tumour, the intercostal space over the affected site becomes rigid. Rigidity of the chest increases in general in the aged due to ossification of the costal cartilages, development the lung emphysema, and also with filling of both pleural cavities with fluid. Increased resistance of the chest can then be felt during examining the chest by compression in both the anteroposterior and lateral directions.
Palpation is used for determining the strength of voice conduction to chest surface {fremitus vocalis s. pectoralis). Vocal fremitus depends on the conduction of voice sounds through the respiratory tract.
The palms of the hands placed on the symmetrical parts of the chest and the patient is asked to i loudly a few words (with the letter ‘r’ in them to intensify vibration). The doctor can ask the patient to repeat words, such as “ninety-nine”, “one, two, three,” “eee-eee”. The patient should speak the words with a voice of uniform intensity. The voice should be as low as possible since voice vibrations are better transmitted by the air column in the trachea and the bronchi to the chest wall in this case. Vibrations are felt as the hands move symmetrically on either side of the sternum and vertebral column.
Fremitus vocalis can also be determined by one hand as as well: the palm of the examining hand should be placed alternately on the symmetrical parts of the chest.
Determination of vocal fremitus (position of examiner’s hands)
. In general vocal fremitus is the most intense in the regions of the thorax where the trachea and bronchi are the closest to the surface, particularly along the sternum between the first and second ribs and posteriorly between the scapulae. Progressing downward, the sound decreases and is least prominent at the base of the lungs.
Vocal fremitus is of about the same intensity in the symmetrical parts of the chest of a healthy person. Vocal vibrations are louder in the upper parts of the chest and softer in its lower parts. Moreover, voice conduction is better in men with low voice and thin chest; the vibrations are weaker in women and children with higher voice (and also in persons with the well developed subcutaneous fat tissues). Vocal fremitus can be stronger or weaker (or in some cases it can even be impalpable) in pathological conditions of the respiratory organs. In focal affections, vocal fremitus becomes unequal over symmetrical parts of the chest.
Vocal fremitus is intensified when a part of the lung or its whole lobe becomes airless and more uniform (dense) because of a pathological process. According to the laws of physics, dense and uniform bodies conduct sound better than loose and non-uniform. Induration (consolidation) can be due to various causes, such as acute lobar pneumonia, pulmonary infarction, tuberculosis, accumulation of air or fluid in the pleural cavity, etc. Vocal fremitus is also intensified in the presence in the pulmonary tissue of an air cavity communicated with the bronchus.
Vocal fremitus becomes weaker:
(1) when liquid or gas are accumulated in the pleural cavity; they separate the lung from the chest wall to absorb voice vibrations propagating from the vocal slit along the bronchial tree;
(2) in complete obstruction of the bronchial lumen by a tumour which interferes with normal conduction of sound waves to the chest wall;
(3) in asthenic emaciated patients (with weak voice);
(4) in significant thickening of the chest wall in obesity.
Low-frequency vibrations due to pleural friction (friction fremitus) in dry pleurisy, crepitation sounds characteristic of subcutaneous emphysema of the lungs, vibration of the chest in dry, low (low-pitch buzzing) rales can also be determined by palpation.
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Decreased vocal fremitus in the upper airway may indicate a) the obstruction of a major bronchus, b) pneumo-, hydro-, haemothorax, c) emphysema of lungs, d) adiposity can also be the cause of decreased vocal fremitus.
The voice of fremitus is increased a) in pneumonia, b) in abscess, b) in atelectasis, c) in cavern.
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Absence of fremitus usually indicates obstruction of a major bronchus, which may occur as the result of aspiration of a foreign body.
Decreased or absent fremitus is always recorded and reported for further investigation. During palpation other vibrations that indicate pathologic conditions are noted. One is a pleural friction rub, which has a grating sensation. It is synchronous with respiratory movements and is the result of opposing surfaces of the inflamed pleural lining rubbing against one another,
Percussion as a method of examination
Percussion is performed to evaluate the size, borders, and consistency of some internal organs; to detect tenderness; and to determine the extent of fluid in a body cavity. There are two percussion techniques: direct and indirect.
Direct percussion involves striking a finger or hand directly against the client’s body. The doctor may use direct percussion technique to evaluate the sinus of an adult by tapping a finger over the sinus, or to elicit tenderness over the kidney by striking the costovertebral angle (CVA) directly with a fist.
Indirect percussion requires both hands and is done by different methods depending on which body system is being assessed. Indirect fist percussion of the kidney, for example, involves placing the nondominant hand palm down (with fingers together) over the CVA and gently striking the fingers with the lateral aspect of the fist of the dominant hand.
Indirect percussion of the thorax or abdomen is performed by placing the distal aspect of the middle finger of the nondominant hand against the skin over the organ being percussed. This finger is sometimes referred to as the pleximeter. The other fingers of that hand are spread apart and slightly elevated off the client’s skin so that they do not dampen the vibration. With the tip of the middle finger of the dominant hand (the plexor), the examiner strikes the distal interphalangeal joint, or just distal to the joint, that lies against the client’s skin. The tip of the striking finger hits the middle finger, which is against the skin, between the cuticle and first joint. Some examiners use both the index and middle fingers as plexors. The wrist must be relaxed and loose while the . pleximemer remains stationary. Rebound the plexor finger as is it strikes the pleximeter so that the vibration is not lost. Listen for the vibrations created by one finger strikes to-other. Tapping produces a vibration 1.5 to 2 inches (4 to ~ deep in body tissue and subsequent sound waves). Per- two or three times in one location before moving to an-other position. Stronger percussion will be needed for obese or very – obese clients, because thickness of tissue can impair the vibrations; the denser the tissue, the quieter the percussion.
Five percussion tones are described:
– Tympanic isloud, high-pitched sound heard over the abdomen.
– Resonance is heard over normal lung tissue, whereas
– hyper-resonance is heard in overinflated lungs (as in emphysema).
– – Dullness is heard over the liver, and
– – flatness is heard over bones and muscle.
Detecting sound changes is easier when moving from resonance to dullness (e.g., from the lung to the liver). Indirect percussion can be mastered with practice.
Immediate percussion by different methods: generally adopted method; by Yanovsky; by Obrastsov
The lungs are percussed in order to evaluate the densities of the underlying organs. Resonance is heard over all the lobes of the lungs that are not adjacent to other organs. Dullness is heard beginning at the fifth interspace in the right midclavicular line. Percussing downward to the end of the liver, a flat sound is heard because the liver no longer overlies the air-filled lung. Cardiac dullness is felt over the left sternal border from the second to the fifth interspace medially to the midclavicular line. Below the fifth interspace on the left side, tympany results from the air-filled stomach. Deviations from these expected sounds are always recorded and reported.
Physical buckgrounds of percussion.
The organs and tissues lying beneath the percussed area begin vibrating and these vibrations are transmitted to the surrounding air. Liquids and airless tissues give dull sounds such as the percussed femur. The properties of each particular percutory sound depend on the amount of air or gas in it.
Percussion Tones
|
ORGANS PERCUSSED |
TONE |
INTENSITY |
PITCH |
DURATION |
DUALITY |
|
lungs |
Resonant |
Loud |
Low |
Long |
Hollow |
|
bone and muscle |
Flat |
Soft |
High |
Short |
Extremely dull |
|
spleen and liver borders |
Dull |
Medium |
Medium high |
Medium |
Thudlike |
|
stomach and gas bubbles |
Tympanic |
Loud |
High |
Medium |
Drumlike |
|
– intestines |
|
|
|
|
|
|
air trapped in lung (emphysema) |
Hyperresonant |
Very loud |
Very low |
Longer |
Booming |
Mediate and immediate percussions
Percussion in done by tapping with a plexor on a pleximeter placed on the body, or by a finger on anothes finger is named mediate percussion. In immediate percussion the examined part of the body is striken directly by the soft tip of the index finger.
Percussion of the chest
In comparative percussing the chest, the anterior lung is percussed from apex to base, usually with the patient in the supine or sitting position. Each side of the chest is percussed in sequence in order to compare the sounds, such as the dullness of the liver on the right side with the tympany of the stomach on the left side. When percussing the posterior lung, the procedure and sequence are the same, although the patient should be sitting. Normally only resonance is heard when percussing the posterior thorax from the shoulder to the eighth or tenth rib. At the base of the lungs dullness is heard as the diaphragm is percussed.
The rules and technique of comparative percussion
A certain sequence is followed in comparative percussion. Percussion sounds over the lung apices (in the front) on the symmetrical points of the chest are first compared; the pleximeter finger is placed parallel to the clavicle. The plexor finger is then used to strike the clavicle which is used as a pleximeter in this case. During percussion of the lungs below the clavicle, the pleximeter finger is placed in the interspace at the strictly symmetrical points of the left and right sides of the chest. The plexor finger is then used to strike the clavicle which is used as a pleximeter in this case. During percussion of the lungs below the clawicle, the pleximeter finger is placed in the interspace at the strictly symmetrical points of the left and right sides of the chest. The percussion sounds are compared only to the level of the 4th rib along the medioclavicular line (and medially). The heart lying below this level changes the percussion sound. For comparative percussion of the axillary region, the patient should raise his arms and clamp the hands at the back of the head. Comparative percussion of the lungs on the back begins with suprascapular areas. The pleximeter finger is placed horizontally, while during percussion of the regions between the scapulae, the pleximeter should be vertical. The patient should cross his arms on the chest to displace the scapulae anteriorly (away from the backbone). During percussion of the points lying below the scapulae, the pleximeter should again be horizontal; in the interspace it should be placed parallel to the ribs
The mechanism of development of pulmonary sound, dull and thympanic sounds
The percussion sound can change in pathological processes because of the decreased content or full absence of air in a part of the lung, and because of the pleural fluid (transudate, effusion, blood), increased airiness of the lung tissue, and the presence of air in the pleural cavity (pneumothorax).
The amount of air in the lungs decreases in
(1) pneumosclerosis, fibrous-focal tuberculosis,
(2) pleural adhesion or obliteration of the pleural cavity which interferes with normal distention of the lung during inspiration; the difference in the percussion sound will be more pronounced at the inspiration level and weaker during the expiration;
(3) lobular and especially confluent pneumonia, in which pulmonary tissue alternates with consolidations;
(4) considerable oedema of the lungs, especially in the inferiolateral regions due to insufficient contractility of the left ventricle;
(5) compression of the pulmonary tissue by the pleural fluid (compression atelectasis) above the fluid level;
(6) complete obstruction of the large bronchus with a tumour and gradual resorption of air from the lungs below the closure of the lumen (obstructive atelectasis). Clear pulmonary sounds I become shorter and higher (i.e. duller) in the mentioned pathological conditions. If these conditions are attended by decreased tension in the elastic elements of the pulmonary tissue, e.g. in the presence of compression or obstructive atelectasis, the sound over the atelectatic zone becomes dull with a tympanic tone. This sound can also be heard during percussion of a patient with acute lobar pneumonia at its first stage, when the alveoli of the affected lobe, in addition to air, contain also a small amount of fluid.
A complete absence of air in the entire lobe of the lung or its part (segment) is observed in the following cases:
(a) acute lobar pneumonia at the consolidation stage, when the alveoli are filled with the inflammatory exudate containing fibrin;
(b) formation in the lung of a large cavity, which is filled with the inflammatory fluid (sputum, pus, echinococcous acid, etc.), or heterogeneous airless tissue (tumour
(c) accumulation of fluid in the pleural cavity (transudate, exudate, blood). Percussion over airless parts of the lung or over fluid accumulated in the pleural cavity gives a soft short and high sound which is called dull or, by analogy with the percussion sounds of airless organs and tissues (liver, muscles), liver dullness. But the absolute dullness identical to the percussion sound of the liver can only be heard in the presence of a large amount of fluid in the pleural cavity.
The amount of air in the lung increases in emphysema. The percussion sound in lung emphysema is louder than the dull tympanic sound because of the increased airiness of the pulmonary tissue and decreased elasticity of the tense pulmonary tissues; but the tympanic character is preserved. The percussion sound resembles the one produced by a stroke on a box; hence the name bandbox sound.
The amount of air held inside the lung increases with formation in it of a smooth-wall cavity filled with air and communicated with the bronchus (abscess, tuberculotic cavern). The percussion sound over this area will be tympanic. If the cavity is small and situated deeply in the chest, vibrations of the pulmonary tissue will not reach this cavity and no tympanic sound will be heard. Such a cavity will only be revealed by roentgenoscopy. The sound over a very large smooth-wall cavity in the lung (6-8 cm in diameter) will be tympanic, resembling a stroke on a metal (metallic percussion sound). If this cavity is located superficially and is communicated with the bronchus through a narrow slit, the percussion sound will be soft and will resemble that of a cracked pot (hence the name—cracked-pot sound).
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The pathological dullness is heard in cause of a) pneumonia, b) hydro-, haemothorax, c) pulmonary edema, d) lung or mediastinal tumor. The banbox is heard in cause of a) emphysema of lungs, b) cavern of lung, c) abscess of lung, d) pneumothorax, e) bronchial asthma, f) asthmatic bronchitis.
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Topographic percussion
In topographic percussing the chest, the doctor looks for the lungs’ borders in the main lines, the location of the apex of the lung and width of Kroenig’s areas.
In topographic percussion the margin of the lung is assessed from the side of resonance sound.
The upper margin of the lung (the location of the apex of the lung) is determined by percussions from the clavicle to the neck. The apex of each lung rises about 2 to 4 cm above the inner third of the clavicles in front of the body At the back we examine the location of the apex of the lung by percussions from the scapula axis to the seventh cervical vertebra. Normally, the upper border of the lung is in the seventh cervical vertebra at the back.
The width of Kroenig’s areas is determined by percussions from the middle of muscle trapezium to each direction (to neck and shoulder) to disappearance of the resonance. Normally, the width of Kroenig’s areas is 3-5 cm.
The excursion of the lung is the distance between the lower costal margin of the lungs in the maximum inspiration and maximum expirations. Normally, the excursion of the lung is 2-6 cm.
The rules of the topographic percussion
During topographic percussion of lungs one should apply such rules as follows
– the finger-pleximeter should be placed parallel to the border of the organ one is seeking for;
– percussion should be carried out from resonans pulmonary sound to dull one.
– If the lungs’ borders has being determined, they should be marked on the edge of the finger-pleximeter from the side of resonans pulmonary sound.
2. Definition of height of the lungs’ apexes.
The lungs’ apexes should be determined on anterior and posterior surface of the chest. To find out the height of the lungs apexes anteriorly percuss from the midpoint of each clavicle parallel to their axis in progressive steps downwards as well as quite medially untill dull percussiootes will be heared. Posteriorly percussion should be carried out from the center of suprascapular area in direction to the point, placed on 3-4 cm laterally to the 7th cervical spinous processus. Iorm the apex of each lung rises anteriorly about 2-4 cm above the inner third of the clavicle, posteriorly – is placed approximately at the level of the 7th cervical spinous processus.
Technique of Kroenig’s area width definition
The locations of the lungs apexes can be mentally projected onto the each shoulder – so-called Krenig’s area. To determine this zone one should use a quiet percussion, moving the finger-pleximeter from the center of trapezoid muscle across the top of each shoulder in direction both to the neck and to the shoulder joint. Percuss across the top of each shoulder to identify the approximately 5-cm band of resonance overlying each lungs apex. In healthy persons the width of dullness makes approximately 3-8 cm.
The upper border of the lung and width of the Kroenig’s area can vary depending on the amount of air in the apices. If the amount of air is high (for example, due to emphysema) the apices increase in size and move upwards. The Kroenig’s area widens accordingly. The presence of connective tissue in the lungs apex (which usually develops during inflammation as in tuberculosis or pneumonia or inflammatory infiltration) decreases the airness of the pulmonary tissue. The upper border of the lung lowers and the width of the Kroenig’s area decreases.
Determination of the lower lungs borders and their mobility
To determine the lower lungs borders one should held the pleximeter finger parallel to the expected border of diaphragmatic dullness, percuss in progressive steps downwards on parasternal, midclavicular, anterior axillary, midaxillary, posterior axillary, scapular and paravertebral lines from the right and left side. Identify the level of diaphragmatic dullness on each side during quiet respiration. This level is often slightly higher on the right. Anteriorly the low border of the left lung on parasternal and midclavicular lines is not distinguished because of heart dullness.
The lower border of the right lung is as a rule at the point of transition of the clear pulmonary resonance to dullness (lung-liver border). In exceptional cases, when air is present in the abdominal cavity (e.g. in perforation of gastric or duodenal ulcer), liver dullness may disappear. The clear pulmonary resonance will then convert to tympany. The lower border of the left lung by the anterior and midaxillary lines is determined by the transition of clear pulmonary resonance to dull tympany. This is explained by the contact between the lower surface of the lung (through the diaphragm) and a small airless organ, such as the spleen and the fundus of the stomach, which give tympany (Traube’s space).
The position of the lower border of the lungs can vary in various pathological conditions that develop in the lungs, the pleura, in diaphragm, and the abdominal viscera. The border can both rise and lower from the normal level. This displacement can be uni- or bilateral.
Bilateral lowering of the lower border of the lungs can occur in acute and chronic dilation of the lungs (attack of bronchial asthma and emphysema of the lungs, respectively) and also in sudden weakening of the tone of the abdominal muscles and lowering of the abdominal viscra (splanchnoptosis). Unilateral lowering of the lower border of the lungs can be due to vicarious (compensatory) emphysema of one lung with inactive tion of the other lung (pleurisy with effusion, hydrothorax, pneumothorax hemiparesis of the diaphragm).
The elevation of the lower border of the lungs is usually unilateral and I occurs in (1) shrivelling of the lung due to development of connective tissue (pneumosclerosis); (2) complete obstruction of the lower-lobe bronchus by a tumor which causes gradual collapse of the lung, atelectasis; (3) accumulation of fluid or air in the pleural cavity which displace the lung up wards and medially toward the root; (4) marked enlargement of the liver (cancer, echinococcosis), or of the spleen (chronic myeloleukaemia) Bilateral elevation of the lower borders of the lungs occurs in the presence I of large amounts of fluid (ascites) or air in the abdomen due to an acute perforation of gastric or duodenal ulcer, and also in meteorism.
Key points of projection of the lungs’ low borders on the anterior and posterior chest include the following:
|
Topographic line |
The right lung |
The left lung |
|
Parasternal |
The Vth intercostal space |
– |
|
Midclavicular |
The VIth rib |
– |
|
Anterior axillary |
The VIIth rib |
The VIIth rib |
|
Midaxillary |
The VIIIth rib |
The VIIIth rib |
|
Posterior axillary |
The IXth rib |
The IXth rib |
|
Scapular |
The Xth rib |
The Xth rib |
|
Paravertebral |
At the level of the 11th thoracic spinous processus |
At the level of the 11th thoracic spinous processus |
Topographic lines on the chest
After determining the lower border of the lungs respiratory mobility of pulmonary borders should be determined by percussion during forced inspiration and expiration. The lungs lower borders mobility can be active or passive.
The active mobility is those observed at respiration, passive – at changes of patient’s position. Active mobility is usually measured by the difference in the position of the lower border of the lungs between the two extremes.
The active lower lungs borders mobility can be measured by noting the distance between the levels of diaphragmatic dullness on full expiration and full inspiration, normally around 5-6 cm. Measurements are done by three lines on the right side (midclavicular, axillary, and scapular lines) and two lines on the left side (midaxillary and scapular lines). The normal variation of the lower border of the lungs is described by the figures given in the table. Mobility of the lower border of the left lung by the midclavicular line can not be determined because of the interference of the heart.
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Determination of respiratory mobility of the lower lung border
The active mobility of lungs is quite different on different topographic lines and includes following:
|
Topographic line |
The right lung |
The left lung |
|
Midclavicular |
3-4 cm |
– |
|
Midaxillary |
5-6 cm |
5-6 cm |
|
Scapular |
3-4 cm |
3-4 cm |
Diagnostic importance of lungs borders mobility
The extension of the Kroenig’s area and rising of lungs apexes are observed at lungs emphysema; in the other hand, at tuberculosis, induration of lungs’ parenchima the sizes of lungs apexes decrease.
The location of lower lungs borders varies at various pathological conditions which can develop in lungs as well as in pleura, diaphragm and organs of abdominal cavity. Both descending and raising of lower lungs borders can be present, that phenomenon can be unilateral or bilateral. They descend at emphysema. An abnormally high level of low lungs’ borders one can suggest pleural effusion or a high diaphragm, as well as paralysis or atelectasis.
Auscultation of lungs
Auscultation: Prior to listening over any one area of the chest, remind yourself which lobe of the lung is heard best in that region: lower lobes occupy the bottom 3/4 of the posterior fields; right middle lobe heard in right axilla; lingula in left axilla; upper lobes in the anterior chest and at the top 1/4 of the posterior fields. This can be quite helpful in trying to pin down the location of pathologic processes that may be restricted by anatomic boundaries (e.g. pneumonia). Many disease processes (e.g. pulmonary edema, bronchoconstriction) are diffuse, producing abnormal findings in multiple fields.
1. Put on your stethoscope so that the ear pieces are directed away from you. Adjust the head of the scope so that the diaphragm is engaged. If you’re not sure, scratch lightly on the diaphragm, which should produce a noise. If not, twist the head and try again. Gently rub the head of the stethoscope on your shirt so that it is not too cold prior to placing it on the patient’s skin.
2. The upper aspect of the posterior fields (i.e. towards the top of the patient’s back) are examined first. Listen over one spot and then move the stethoscope to the same position on the opposite side and repeat. This again makes use of one lung as a source of comparison for the other. The entire posterior chest can be covered by listening in roughly 4 places on each side. Of course, if you hear something abnormal, you’ll need to listen in more places.
3. The lingula and right middle lobes can be examined while you are still standing behind the patient.
4. Then, move around to the front and listen to the anterior fields in the same fashion. This is generally done while the patient is still sitting upright. Asking female patients to lie down will allow their breasts to fall away laterally, which may make this part of the examination easier.
Listen to the respiratory rate, including rhythm and depth of respirations. Compare rate with normal respiratory rates for the age of the client.
Auscultate the lungs, listening to inspiration and expiration at each site.
Auscultate the anterior lung fields. Listen for abnormal sounds, including rales, rhonchi, or wheezes.
Normal and abnormal respiratory patterns
A few additional things worth noting.
1. Don’t get in the habit of performing auscultation through clothing.
2. Ask the patient to take slow, deep breaths through their mouths while you are performing your exam. This forces the patient to move greater volumes of air with each breath, increasing the duration, intensity, and thus detectability of any abnormal breath sounds that might be present.
3. Sometimes it’s helpful to have the patient cough a few times prior to beginning auscultation. This clears airway secretions and opens small atelectatic (i.e. collapsed) areas at the lung bases.
4. If the patient cannot sit up (e.g. in cases of neurologic disease, post-operative states, etc.), auscultation can be performed while the patient is lying on their side. Get help if the patient is unable to move on their own. In cases where even this cannot be accomplished, a minimal examination can be performed by listening laterally/posteriorly as the patient remains supine.
- Requesting that the patient exhale forcibly will occasionally help to accentuate abnormal breath sounds (in particular, wheezing) that might not be heard when they are breathing at normal flow rates.
In thin bony chests, the bell may give a more airtight fit and is less likely to trap hairs underneath, which produce a crackling sound. The breath sounds are produced in the large airways, transmitted through the airways and then attenuated by the distal lung structure through which they pass. The sounds you hear at the lung surface are therefore different from the sounds heard over the trachea and are modified further if there is anything obstructing the airways, lung tissue, pleura or chest wall. When reporting on auscultatory changes, you must distinguish between the breath sounds and the added sounds. Breath sounds are termed either vesicular or bronchial and the added sounds are divided into crackles, wheezes and rubs.
Vesicular breathing sounds
The breath sounds are produced in the large airways, transmitted through the airways and then attenuated by the distal lung structure through which they pass.
expiration
Inspiration
The sounds you hear at the lung surface are therefore different from the sounds heard over the trachea and are modified further if there is anything obstructing the airways, lung tissue, pleura or chest wall. When reporting on auscultatory changes, you must distinguish between me breath sounds and thVaddcd sounds. Breath sounds arc- termed either vesicular or bronchial and the Vesicular breath sounds This is the sound heard over normal lungs, it has a rustling quality and is heard on inspiration and the first part of expiration (Fig. 5,46). Reduction in vesicular breath sounds can be expected with airways obstruction as in asthma, emphysema or tumour. The so-called ‘silent chest’ is a sign of severe asthma: so little air enters the lung that no sound is produced. The breath sounds can be strikingly reduced in emphysema, particularly over a bulla. Generalised reduction in breath sounds also occurs with a thick chest wall or obesity. Anything interspersed between the lung and the chest wall (air, fluid or pleural thickening) will reduce the breath sounds: this is likely to be unilateral and therefore more easily detected. Avoid the term ‘diminished air entry’ when you mean diminished breath sounds. The two are not necessarily synonymous.
Bronchial breathing
Bronchial breathing causes much confusion because the essential feature of bronchial breathing, the quality of the sound, is difficult or impossible to put into words. Traditionally, it is described by its timing as occurring in both inspiration and expiration with a gap in between. The diagram of bronchial breath sounds is:
expiration
inspiration
In this way it is contrasted with vesicular breathing. These features are undoubtedly true but lead to the confusion in the mind of the student that if anything is heard in middle or late expiration it must be bronchia] breathing. Many normal people and individuals with airways obstruction have prolonged expiratory component to the breath sounds (this is sometimes designated “bronchovesicular” but this term increases the confusion rather than diminishing it). It is best to forget about the timing and concentrate on the essential feature, the quality of the sound. It can be mimicked to some extent by listening over the trachea with the stethoscope, although a better imitation can be obtained by putting the tip of your tongue on to roof of your mouth and breathing in and out through the open mouth. Bronchial breathing is heard when sound generated in the Central airways is transmitted more or less unchanged through the lung substance. This occurs when the lung substance itself is solid as in consolidation but the air passages remain open. Sound is conducted normally to the small airways but then instead of being modified by air in the alveoli, the solid lung conducts the sound better to the lung surface and, hence, to the stethoscope. If the central airways are obstructed by say a carcinoma, theo transmission of sound will take place and no bronchial breathing will occur even though the lung may be solid. An exception is seen in the upper lobes. Here, if the bronchi to either lobe are blocked, sounds from the central airways can still be transmitted directly from die trachea through the solid lung to the chest wall.
The main cause of bronchial breathing is consolidation particularly from pneumonia, so much so that in the minds of most clinicians the three terms are synonymous. Lung abscess, if near the chest wall, can cause bronchial breathing probably because of the consolidation around it. Dense fibrosis is an occasional cause. Breath sounds over an effusion will be diminished but bronchial breathing may be heard over its upper level perhaps because the effusion compresses the lung. Bronchial breathing is only heard over a collapsed lung if the airway is patent. This is rare as the collapse is usually caused by an obstructing carcinoma. Nevertheless, there is an exception with the upper lobes (see above). Bronchial breathing has been divided into tubular, cavernous and amphoric but attempts to score points on ward rounds by using these terms are best left to others.
Absent or diminished breath sounds are always an abnormal finding warranting investigation. Fluid, air, or solid masses in the pleural space all interfere with the conduction of breath sounds (pneumonia, pneumo-, hydro-, haemothorax, tumor of lung or mediastinal, emphysema of lungs, atelectasis, airways obstruction, a foreing body in the bronchus). Diminished breath sounds in certain segments of the lung can alert the doctor to pulmonary areas that may benefit from postural drainage and percussion. Increased breath sounds following pulmonary therapy indicate improved passage of air through the respiratory tract.
Voice sounds are also part of auscultation of the lungs. Normally voice sounds or vocal resonance is heard, but the syllables are indistinct. They are elicited in the same manner as vocal fremitus, except that the doctor listens with the stethoscope. Consolidation of the lung tissue produces three types of abnormal voice sounds.
1. Whispered pectoriloquy, in which the child whispers words and the nurse, hears the syllables.
2. Bronchophony, in which the child speaks words that are not distinguishable but the vocal resonance is increased in intensity and clarity.
3. Egophony, in which the child says “ee,” which is heard as the nasal sound “ay” through the stethoscope.
Decreased or absent vocal resonance is caused by the same conditions that affect vocal fremitus.
Various pulmonary abnormalities produce adventitious sounds that are not normally heard over the chest. They are not alterations of normal breath sounds but rather sounds that occur in addition to normal or abnormal breath sounds. They are often referred to as the three “R’s”: rales (from the French word meaning “rattle”), rhonchi, and rubs. Considerable practice with an experienced tutor is necessary to differentiate the various types of adventitious sounds. Often it is best to describe the type of sound heard in the lungs rather than to try and label it correctly.
Rales result from the passage of air through fluid or moisture. They are more pronounced when the child takes a deep breath. Even though the sound may seem continuous, it is actually composed of several discrete sounds, each originating from the rupture of a small bubble. The type of rales is determined by the size of the passageway and the type of exudate the air passes through. They are roughly divided into three categories: fine, medium, and coarse.
Fine rales (sometimes called crepitant rales) can be simulated by rubbing a few strands of hair between the thumb and index finger close to the ear or by slowly separating the thumb and index finger after they have been moistened with saliva. The result is a series of fine crackling sounds. Fine rales are most prominent at the end of inspiration and are not cleared by coughing. They occur in the smallest passageways, the alveoli and bronchioles.
Medium rales are not as delicate as fine rales and can be simulated by listening to the “fizz” from recently opened carbonated drinks or by rolling a dry cigar between the fingers. They are prominent earlier during inspiration and occur in the larger passages of the bronchioles and small bronchi.
Coarse rales are relatively loud, coarse, bubbling, gurgling sounds that occur in the large airways of the trachea, bronchi, and smaller bronchi. Often they clear partially during coughing. They are frequently heard in dying patients because the cough reflex is depressed, allowing thick secretions to accumulate in the trachea and major bronchi. Because they are so common when death is imminent, coarse rales are often called “the death rattle.”
Rhonchi (rales) are sounds produced as air passes through narrowed passageways, regardless of the cause, such as exudate, inflammation, spasm, or tumor. Rhonchi are continuous, since sound is produced as long as air is being forced past an obstruction. Although they are often more prominent during expiration, they are usually present during both phases of respiration. Rhonchi are classified according to pitch as sibilant or sonorous.
Sibilant rhonchi are high pitched, musical, wheezing, or squeaking in character. The wheezing quality is often more pronounced on forced expiration. Sibilant rhonchi are produced in the smaller bronchi and bronchioles.
Sonorous rhonchi are low pitched and often snoring or moaning in character. They are produced in the large passages of the trachea and bronchi. Like coarse rales, they can be partly cleared by coughing. Some clinicians classify sonorous rhonchi as coarse rales, or vice versa.
The other adventitious sound of importance is the pleural friction rub. Its sound can be simulated by cupping one hand to the ear and rubbing a finger of the other hand across the cupped hand. The most common site for a friction rub to be heard is the lower antero-lateral chest wall (between the midaxillary and midclavicular lines), the area of greatest thoracic mobility.
Classifacation and mechanism of origin of dry rales
Dry rales, or rhonchi, may be due to various causes. The main one is constriction of the lumen in the bronchi. Constriction may be total (in bronchial asthma), non-uniform (in bronchitis), or focal (in tuberculosis or tumour of the bronchus). Dry rales can be due to (1) spasms of smooth muscles of the bronchi during fits of bronchial asthma; (2) swelling of the bronchial mucosa during its inflammation; (3) accumulation of viscous sputum in the bronchi which adheres to the wall of the bronchus and narrows its lumen; (4) formation of fibrous tissue in the walls of separate bronchi and in the pulmonary tissue with subsequent alteration of their architectonics (bronchiectasis, pneumosclerosis); (5) vibration of viscous sputum in the lumen of large and medium size bronchi during inspiration and expiration: being viscous, the sputum can be drawn (by the air stream) into threads which adhere to the opposite walls of the bronchi and vibrate like strings.
According to the quality and pitch of the sounds produced, dry rales are divided into sibilant (high-pitched and whistling sounds) and sonorous rales (low-pitched and sonoring sounds). High-pitched rales are produced when the lumen of the small bronchi is narrowed, while low-pitched sonorous rales are generated in stenosis of medium calibre and large calibre bronchi or when viscous sputum is accumulated in their lumen.
Propagation and loudness of dry rales depend on the size of the affected area in the bronchial tree, on the depth of location of the affected bronchi, and the force of the respiratory movements. When the walls of a medium size and large bronchi are affected to a limited extent, rhonchi are insignificant and soft. Diffuse inflammation of the bronchi or bronchospasm arising during attacks of bronchial asthma is attended by both high-pitched sibilant and low-pitched sonorous rales which vary in tone and loudness. These rhonchi can be heard at a distance during expiration.
Classifacation and mechanism of origin of moist rales
Moist rales are generated because of accumulation of liquid secretion (sputum, oedematous fluid, blood) in the bronchi through which air passes. Air bubbles pass through the liquid secretion of the bronchial lumen and collapse to produce the specific cracking sound. This sound can be simulated by bubbling air through water using a fine tube. Moist rales are heard during both the inspiration and expiration, but since the air velocity is higher during inspiration, moist rales will be better heard at this respiratory phase.
Depending on the calibre of bronchi where rales are generated, they are classified as fine, medium and coarse bubbling rales. Fine bubbling rales are generated in fine bronchi and are percepted by the ear as short multiple sounds. Rales originating in the finest bronchi and bronchioles are similar to crepitation from which they should be differentiated. Medium bubbling rales are produced in bronchi of a medium size and coarse bubbling rales in large calibre bronchi, in large bronchiectases, and in pulmonary cavities (abscess, cavern) containing liquid secretions and communicating with the large bronchus. Large bubbling rales are characterized by a lower and louder sound.
Moist rales originating in superficially located large cavities (5-
Depending on the character of the pathology in the lungs, moist rales are subdivided into consonating or crackling, and non-consonating or bubbling rales. Consonating moist rales are heard in the presence of liquid secretions in the bronchi surrounded by airless (consolidated) pulmonary tissue or in lung cavities with smooth walls surrounded by consolidated pulmonary tissue. The cavity itself acts as a resonator to intensify moist rales. Moist consonating rales are heard as if just outside the ear. Consonating rales in the lower portions of the lungs suggest inflammation of :he pulmonary tissue surrounding the bronchi. Consonating rales heard in the subclavicular or subscapular regions indicate tuberculous infiltration or cavern in the lung.
Non-consonating rales are heard in inflammation of bronchial mucosa (bronchitis) or acute oedema of the lung due to the failure of the left chambers of the heart. The sounds produced by collapsing air bubbles in he bronchi are dampened by the “air cushion” of the lungs as they are conducted to the chest surface.
Crepitation
As distinct from rales, crepitation originates in the alveoli. Crepitation is a slight crackling sound that can be imitated by rubbing a lock of hair. The main condition for generation of crepitation is accumulation of a small amount of liquid secretion in the alveoli. During expiration, the alveoli stick together, while during inspiration the alveolar walls are separated with difficulty and only at the end of the inspiratory movement. Crepitation is therefore only heard during the height of inspiration.
Crepitation is mainly heard in inflammation of the pulmonary tissue, e.g. at the first (initial) and third (final) stages of acute lobar pneumonia, when the alveoli contain small amounts of inflammatory exudate, in infiltrative pulmonary tuberculosis, lung infarction, and finally in congestions that develop due to insufficient contractile function of the left-ventricular myocardium or in marked stenosis of the left venous orifice of the heart. Crepitation can be heard in the inferolateral portions of the lungs of aged persons during first deep inspirations, especially so if the patient was in the recumbent position before auscultation. The same temporary crepitation can be heard in compressive atelectasis. During pneumonia, crepitation is heard over longer periods and disappears when a large amount of inflammatory secretion is accumulated in the alveoli or after its complete resolution.
Auscultatory characteristics of pleural friction sound
Pleural friction sound is a peculiar adventitious noise generated by friction of visceral and parietal layers of the pleura during breathing. Fibrin is deposited in inflamed pleura to make its surface rugh; moreover, cicatrices, commissures, and bands are formed between pleural layers at the focus of inflammation. Tuberculosis or cancer are also responsible for the friction sounds.
Pleural friction sounds are heard during both inspiration and expiration. The sounds are differentiated by intensity, or loudness, length and localisation. During early dry pleurisy the sounds are soft and can be imitated by rubbing silk or fingers in the close vicinity of the hair. The character of pleural friction sound is altered during the active course of dry pleurisy. It can resemble crepitation or fine bubbling rales sometimes crackling of snow). In pleurisy with effusion, during the period of rapid resorption of exudate, the friction sound becomes coarser due to massive deposits on the pleural surfaces. This friction (to be more exact, brations of the chest) can be even identified by palpation of the chest.
The time during which pleural friction sound can be heard varies with causes. For example, in rheumatic pleurisy pleural friction is only heard during a few hours; after a period of quiescence it reappears. Pleural friction persists for a week and over in dry pleurisy of tuberculous aetiology id pleurisy with effusion at the stage of resorption. Pleural friction sounds can be heard in some patients for years after pleurisy because of rge cicatrices and roughness of the pleural surfaces.
The point over which pleural friction can be heard depends on the focus of inflammation. Most frequently it is heard in the inferolateral parts of e chest, where the lungs are most mobile during respiration. In rare cases is sound can be heard over the lung apices, when they are affected by berculosis with involvement of the pleural membranes.
Bronchophony
This is the voice conduction by the larynx to the chest, as determined by auscultation. But as distinct from vocal fremitus, the words containing sounds ‘r’ or ‘ch’ are whispered during auscultation. In physiological conditions, voice conducted to the outer surface of the chest is hardly audible on either side of the chest in symmetrical points. Exaggerated bronchophony (like exaggerated vocal fremitus) suggests consolidation of the pulmonary tissue (which better conducts sound waves) and also cavities in the lungs which act as resonators to intensify the sounds. Bronchophony is more useful than vocal fremitus in revealing consolidation foci in the lungs of a patient with soft and high voice.
Examination of gastrointestial tract
OESOPHAGUS
Complaints. Dysphagia (difficult passage of food via the oesophagus) is the most frequent symptom of oesophageal pathology. The patient feels difficulty in swallowing (mostly solid food); the food bolus sometimes stops in the oesophagus and the patient feels pain and oesophageal distention. Dysphagiaucan be due to organic or functional narrowing of the oesophagusfOrganic stenosis develops gradually and progresses in cancer, and cicatricial stenosis of the oesophagus. Solid food first passes with difficulty, then the patient feels difficulty in swallowing soft, and then liquid food. When cancer tumour disintegrates, patency of the oesophagus may be restored almost completely. Dysphagia develops immediately in the presence of a foreign body or if the oesophagus is burnt. Dysphagia may also develop due to compression from outside by an aortic aneurysm or mediastinal tumour.
Functional narrowing of the oesophagus is explained by muscular spasms caused by reflex disorders in innervation of the oesophageal muscles, or by neurosis. As distinct from organic dysphagia, functional dysphagia more often occurs in paroxysms when food passes the oesophagus. Sometimes solid food passes more readily than liquid.
Pain occurs in acute inflammation of the oesophageal mucosa (oesophagitis) and in burns. The patient usually feels pain by the course of the entire oesophagus, both with and without swallowing; pain may radiate into the interscapular region.
Patients with achalasia of the cardia (cardiospasm) may have spontaneous attacks of pain, usually during night. Pain is quite severe; it radiates into the back, upwards by the oesophagus, into the neck, the jaws, and continues for minutes and even hours. In the presence of hiatus hernia and gastroesophageal reflux, pain may radiate into the left side of the chest and simulate heart diseases.
Oesophageal vomiting occurs in considerable narrowing of the oesophagus. Food is accumulated over the constricted point, in the wider portion of the oesophagus, and is expelled by antiperistaltic contractions of the muscles. Oesophageal vomiting differs from gastric vomiting in the following: it occurs without nausea and is preceded by the feeling of food retained behind the sternum the vomitus includes unaltered (non-digested) food which contains neither hydrochloric acid (gastric juice) nor pepsin; the vomitus containing food that has been taken long time ago has foulodour; taken food can be retained for long periods in the presence of oesophageal diverticulum or degrading cancer.
Regurgitation is the return of swallowed food into the mouth due to oesophageal obstruction. Regurgitation sometimes occurs in neuropathic patients in whom it becomes a habitual symptom or a result of cardiospasm.
Hypersalivation occurs in oesophagitis, cicatricial narrowing of the oesophagus or in cancerous stenosis as a result of the oesophagosalivary reflex.
A foul breath may be due to a cancer tumour of the oesophagus or congestion and decomposition of food in cardiospasm.
Heartbearn (pyrosis) is a specific burning sensation behind the sternum associated with regurgitation of gastric contents into the inferior portion of the oesophagus. This is the cause of the so-called reflux oesophagitis.
Haemorrhage can be due to uicer of the oesophagus, injury to the oesophagus by a foreign body, degradation of a tumour, bleeding of dilated oesophageal veins (which occurs in congestion of blood in the portal vein system) and also bleeding of the mucosa due to small lacerations of the vessels in the oesophagogastric junction in straining and vomiting (Mallory- Weiss syndrom)
STOMACH
Complaints. Patients with diseases of stomach complain of poor appetite, perverted taste, regurgitation, heartbearn, nausea, vomiting, and the feeling of overfilled stomach after meals are the group of the so-called dyspeptic complaints. These symptoms may be observed in diseases of some other organs and systems. Determining the specific character of each symptom is important during inquiry of the patient.
Deranged ( poor or increased) appetite occurs in infectious diseases,metabolic disorders, ets.poor appetite or itscomplete absence (anorexia)is usually characteristic of gastric cancer. This symptom is often an early sign of cancer. Appetite often increases in peptic ulcer, especially in duodenal ulcer. Loss of appetite should be differentiated from cases when the patient abstains from food for fear of pain (cibophobia)/ This condition often occurs in subjects with gastric ulcer, though their appetite is increased.
Perverted appetite thet sometimes occurs in patients is characterized by the desire to eat inedible materials suuch as charcoal, chalk, kerosine, ets.
Appetite is perverted in pregnant women and in persons suffering from achlorhydria. Some patients with cancer of the stomach or some other organs often feel aversion to meat. The developmental mechanism of appetite is connected with excitation of the food centre (according to
Taste may be perverted due to the presence of unpleasant taste in the mouth and partial loss of taste in an individual. It can often be associated with some pathology in the mouth, e.g. caries or chronic tonsillitis. A coated tongue can be another cause of unpleasant taste in the mouth.
Regurgitation usually implies two phenomena: a sudden and sometimes loud uprise of wind from the stomach or oesophagus (eructation), and the return of swallowed food into the mouth (sometimes together with air). Regurgitation depends on contraction of the oesoohageal muscles with the openn cardia. Regurgitation may be due to air swallowing (aerophagy). It is heard at a distance and occurs in psychoneurosis. In the presence of motor dysfunction of the stomach, fermentation and putrefaction of food with increased formation of gas occur in the stomach (the phenomenon otherwise absent iorm). In abnormal fermentation in the stomach, the eructated air is either odourless or smells of bitter oil, which is due to the presence of butyric, lactic and other organic acids that are produced during fermentation in the stomach. In the presence of abnormal putrefaction, the helched air has the odour of rotten eggs (hydrogen sulphide). Bitter belching indicates intensive degradation of proteins. Belching is characteristic of stenosed pylorus with great distention of the stomach and significant congestion in it. Acid regurgitation is usually associated with hypersecretion of gastric juice and occurs mostly during pain attacks in ulcer. But it can also occur iormal or insufficient secretion of the stomach in the presence of insufficiency of the cardia (when the stomach contents are regurgitated into the oesophagus). Bitter regurgitation occurs in cases with belching up of bile into the stomach from the duodenum, and also in hyperchlorhydria; bitterness depends on the bitter taste of peptones.
Pyrosis is otherwise known as heartburn, i.e. burning pain in the epigastric and retrosternal region. Heartburn arises in gastro-oesophageal reflux, mostly in the presence of gastric hyperacidity in various diseases of the alimentary tract (e.g. peptic ulcer or cholecystitis), hiatus hernia, and sometimes in pregnancy. Heartburn in healthy subjects can be due to hypersensitivity to some foods.
Nausea, the reflectory act associated with irritation of the vagus nerve, is an indefinite feeling of sickness and sensation of compression in the epigastrium. Nausea is often attended by pallidness of the skin, general weakness, giddiness, sweating, salivation, fall in the arterial pressure, cold in the limbs, and sometimes semisyncopal state. Nausea often (but not necessarily) precedes vomiting. The mechanism of nausea is not known. Its frequent association with vomiting suggests that it might be the early sign of stimulation of the vomiting centre. The leading role in the development of nausea is given to the nervous system and also the tone of the stomach, the duodenum, and the small intestine. Nausea may develop without any connection with diseases of the stomach, e.g. in toxaemia of pregnancy, renal failure, deranged cerebral circulation, and sometimes in healthy people in the presence of foul odour (or in remembrance of something unpleasant). Some diseases of the stomach are attended by nausea, e.g. acute and chronic gastritis or cancer of the stomach. Nausea associated with gastric pathology usually occurs after meals, especially after taking some pungent food. Nausea often develops in secretory insufficiency of the stomach.
Vomiting (emesis) occurs due to stimulation of the vomiting centre. This is a complicated reflex through the oesophagus, larynx and the mouth (sometimes through the nose as well). Vomiting may be caused by ingestion of spoiled food, by seasickness, or irritation arising inside the body (diseases of the gastro-intestinal tract, liver, kidneys, etc.). In most cases vomiting is preceded by nausea and sometimes hypersalivation. Factors causing the vomiting reflex are quite varied. This can be explained by the numerous connections that exist between the vomiting centre (located in the medulla oblongata, in the inferior part of the floor of the 4th ventricle) and all bodily systems. Depending on a particular causative factor, the following can be differentiated: (1) nervous (central) vomiting; (2) vomiting of visceral aetiology (peripheral or reflex); (3) haematogenic and toxic vomiting.
Vomiting is an important symptom of many diseases of the stomach, but it can be regarded as the symptom of a particular disease only in the presence of other signs characteristic of this disease. Vomiting of gastric aetiology is caused by stimulation of receptors in the gastric mucosa by inflammatory processes (acute or chronic gastritis), in ingestion of strong acids or alkalis, or food acting on the gastric receptors by chemical (spoiled food) or physical (overeating or excessively cold food) routes. Vomiting can also be caused by difficult evacuation of the stomach due to spasms or stenosed pylorus.
If the patient complains of vomiting, the physician should inquire about the time when the vomiting occurred, possible connections with meals, association with pain, the amount and character of the vomited material. Morning vomiting (on a fasting stomach) with expulsion of much mucus is characteristic of chronic gastritis, especially in alcoholics. Hyperacid vomiting in the morning indicates nocturnal hypersecretion of the stomach. Vomiting occurring 10-15 minutes after meals suggests ulcer or cancer of the cardial part of the stomach, or acute gastritis. If vomiting occurs 2-3 hours after meals (during intense digestion) it may indicate ulcer or cancer of the stomach body. In the presence of ulcer of the pylorus or duodenum, vomiting occurs 4-6 hours after meals. Expulsion of food taken a day or two before is characteristic of pyloric stenosis. Patients with peptic ulcer often vomit at the height of pain htus removing it, which is typical of the disease. The odour of the vomit is usually acid, but it can often be fetid (putrefactive processes in the stomach); the odour may be even faecal (in the presence of a faecal fistula between the stomach and the transverse colon).
The vomited material may have acid reaction (due to the presence of hydrochloric acid, in hyperchlorhydria), neutral (in achylia), or alkaline (in the presence of ammonia compounds, in pyloric stenosis, hypofunction of renal function, and also in regurgitation of the duodenal contents into the stomach). Vomitus may contain materials of great diagnostic importance, e.g. blood, mucus (in chrome gastritis), ample bile (narrowing of the duodenum, gastric achylia), and faecal matter. Vomiting may attend acute gastritis, exacerbation of chronic gastritis, gastric neurosis, peptic ulcer, spasm and organic stenosis of the pylorus, and cancer of the stomach.
Pain is the leading symptom in diseases of the stomach. Epigastric pain – not obligatory connected with diseases of the stomach. It should be remembered that the epigastrium is the “site of encounter” of all kinds of pain. Epigastric pain may be due to diseases of the liver, pancreas, and due to hernia of the linea
Paroxysmal, periodical epigastric pain is due to the spasm of the pylorus muscles. It arises under the influence of strong impulses arriving from vagus nerve centre in cerebral cortex dysfunction. The spasm of the pylorus is stimulated by the hyperacidity of gastric juice due to hyperstimulation of the vagus. Depending on the time of paroxysmal pain (after meals), il be early (occurring 30—40 min after meals), late (90—120 min after meals), nocturnal, and hunger pain (which is abated after taking food). If pain occurs after meals stimulating secretion of gastric juice (bitter, pungent, spicy or smoked foods), this indicates the leading role of hypersecretion in its aetiology. The pain then localizes in the epigastrium, radiates to the back, and is rather intense; it is abated after vomiting and taking alkali or foods that decrease acidity of gastric juice, and also after taking antispastic preparations and applying hot-water bottle (which removes spasms)
A seasonal character of pain, i.e. development of periodic pain duringl spring and autumn, is characteristic of peptic ulcer, especially if the process is localized in the peripyloric region. Permanent boring pain is usually caused by stimulation of the nerve elements in the mucous and submucousuii layer of the stomach; the pain is usually intensified after meals and is characteristic of exacerbation of chronic gastritis or cancer of the stomach.
Perigastritis (chronic inflammation of the peritoneum overlyin, stomach and its adhesion to the neighbouring organs) is manifested I developing immediately after taking much food (irrespective of its quality). The full stomach distends to stimulate nerve fibres in the adhesions. In the presence of perigastritis and adhesions between the stomach and the adjacent organs, pain may be caused by any physical strain and when the patient changes his posture.
Gastric haemorrhage is a very important symptom. It manifested by vomiting of blood (haematemesis) or by black tarry stools (melaena). Gastric haemorrhage is usually manifested by the presence of blood in the vomitus. The colour of the vomitus depends on the time duing which the blood is present in the stomach. If the blood wos in the stomach for a long time, the blood reacts with hydrochloric acid of the gastric juice to form haematin hydrochloride. The vomitus looks like coffee grounds. If haemorrhage is profuse (damage to a large vessel) the vomitus contains much scarlet (unaltered) blood. Haematemesis occurs in peptic ulcer, cancer, and polyps, in erosive gastritis, rarely in ssarcoma,tuberculosis and syphilis of the stomach, and in varicosity of the oesophageal veins/ Tarry stools are not an obligatory sign of gastric haemorrage.
INTESTINE
Complaints. The main complaints with intestinal diseases are pain, meteorism (intlation of the abdomen), motor dysfunction of the intestine (constipation and diarrhoea), and intestinal haemorrhage.
Pain. If the patient complains of pain in the abdomen, the following should be established: location of pain, its radiation, intensity, character, duration, and means by which it is lessened. The general signs by which intestinal pain may be differentiated from gastric one are: (1) absence of regular dependence of pain on food taking; the only exception is inflammation in the transverse colon (transversitis): pain develops immediately after meals; the pathogenesis of this pain is connected with reflex peristaltic contractions of the transverse colon when food enters the stomach; (2) close association of pain with defaecation: pain occurs before, during, and (rarely) after defaecation; (3) pain relief after defaecation or passage of gas.
Pain may be boring and spasmodic (intestinal colic). Colicky pain is characterized by short repeated attacks which arise and disappear quite of a sudden. Pain may very quickly change its location, the main site being round the navel. Sometimes pain may arise in other areas of the abdomen. Boring pain is sometimes permanent; it intensifies during cough, especially in the mesenterium or peritoneum are involved. Pain is characteristic of inflammatory diseases of the intestine. As inflammation extends onto the peritoneum, pain is attended by a pronounced muscular defence.
Exact location of the source of pain is very important. Pain in right iliac region occurs in appendicitis, tuberculosis, cancer, or inflammation of the caecum (typhlitis). Acute pain in the left lower abdomen occurs in intestinal obstruction and inflammation of the sigmoid (sigmoiditis).Pain in the umbilical region occurs in inflammation of small intestine (enteritis) and inflammation or cancer of the colon. Pain in the perineal region, and especially during defaecation (with the presence of blood in faeces), is characteristic of the rectum diseases (proctitis, cancer). Pain in intestinal pathology may radiate into the chest; pain associated with affection of the spleen angle of the descending large intestine radiates into the left side of the chest (it is sometimes mistaken for pain attacks of angina pectoris); colics of appendicitic origin radiate into the right leg.
In acute affection of the left portions of the large intestine (dysentery) pain radiates into the sacral area. Thermal procedures, spasmolytycs, passage of gas, and emptying of the bowels can relieve pain or remove it completely.
Intestinal pain is caused by obstruction of intestinal patency and upset motor function. Intestinal pain is mostly caused by spasms ( spasmodic contraction of smooth muscles; hence spastic pain), or by distension of the intestine by gases. Both mechanisms often become involved.
Spastic pain can be due to various causes. Individual predisposition to spastic contractions in general (vegetoneurosis) may be as impotant as irritation originating in the intestine proper, e.g. in enteritis, intestinal tumour, poisoning with arsenic or lead, and also in diseases of the central nervous system (posterior spinal sclerosis).
Pain arising due to intestinal distension by gases, and associated with tension and irritation of the mesentery, differs from spastic pain (1) by the absence of periodicity; it is long-standing and gradually lessens in prolonged inflation; and (2) by exact localization. In intestinal obstruction (complete or partial) colicky pain is combined with almost permanent pain in the abdomen. It is characterized by exact and permanent location ( the umbilical region and large intestine). The pain intensifies with intestynal peristalsis.
Appendicular colic first localizes round the navel and the epygastrium but in several hours (or even on the next day) it descends to the right iliac region where it intensifies gradually. Sometimes the pain arises straight the right iliac region.
Rectal colic, or tenesmus, is also known. It occurs in frequent and painful tenesmus to defaecate and is associated with spasmodic contractions of the intestine and the sphincter ani. Only clots of mucus are sometimes expressed of actual defaecation. Tenesmus occurs in dysentery and other inflammatory or ulcerous diseases, and in cancer of the rectum. Pain associated with defaecation depends on many factors. Pain preceding defaecation is associated with the disease of the descending colon or sigmoid colon. Pain during defaecation is characteristic of haemorrhoids, anal fissures, and cancer.
Meteorism. The patient feels flatulence, inflation, and boring distention of the abdomen. The causes of meteorism are (1) excessive gas formation in the intestine due to ingestion of vegetable cellular tissue and easily tormented food (peas, beans, cabbage, etc.); (2) intestinal motor dysfunc-tion due to decreased tone of the intestinal wall or intestinal obstruction; (3) lowered absorbability of gases by the intestinal wall, the process of gas formation being normal; (4) aerophagia, i.e. excess swallowing of air, with its subsequent propulsion to the stomach and the intestine; (5) hysterical meteorism: the abdomen is rapidly inflated to the size of the abdomen of a pregnant woman at her last weeks; this nervous mechanism is very complicated.
When inquiring the patient, the physician should ask about the character of his nutrition and the site of abdemen inflation (the entire abdomen or only its limited part may be inflated). If inflation is local, it is necessary to ask the patient whether or not inflation occurs always at one and the same area. In intestinal obstruction, the patient feels rumbling sounds inside the abdomen, feels movement of liquid in the intestine, and intense peristaltic movements above the point of obstruction.
Diarrhoea. Frequent and liquid stools is a common sign of intestinal pathology. Diarrhoea occurs in acute and chronic intestinal infections (enteritis, enterocolitis, sigmoiditis, proctitis), in various exogenous intoxications (poisoning with arsenic or mercury), endogenous intoxications (uraemia, diabetes, gout), in endocrine disorders (adrenal dysfunction, thyrotoxicosis), and in hypersensitivity to some foods (allergy).
The mechanism of diarrhoea is very complicated. Different pathogenic factors may prevail in various pathological conditions. Accelerated movement of the liquefied food in the intestine due to peristalsis is among them. Almost undigested food can thus be evacuated. Another factor is disordered absorptive function of the intestine. Affection of the intestinal wall, disordered mechanisms regulating absorption, purgatives and upset water metabolism produce a marked change in the absorption process and are the cause of diarrhoea.
The third cause of liquid stools is inflammation of the intestine. Large quantities of inflammatory secretion stimulating the intestinal receptors are released into the lumen of the intestine to intensify its peristalsis and to impair its absorptive function.
Paradoxical diarrhoea occurs in prolonged constipation due to mechanical irritation of the intestinal wall by hard faecal masses.
Upset equilibrium between the fermentative and putrefactive flora of the intestine is another important factor in the aetiology of diarrhoea. If fermentative flora prevails, fermentative dyspepsia occurs which is characterized by flatulence of the abdomen and semiliquid acid faeces (2— 3 stools a day); the faeces contaiumerous gas bubbles, numerous starch grains, vegetable cellular tissue, and iodophilic microbes. Fermentative dyspepsia develops in connection with deranged digestion of carbohydrates, if they are ingested in excess.
Putrid dyspepsia more often occurs in secretory hypofunction of the stomach. The absence of bactericidal action of gastric juice is connected with the absence of hydrochloric acid; rapid passage of insufficiently digested food from the stomach to the intestine has a negative effect in the first instance on digestion of proteins. This in turn provokes putrid dyspepsia. It is characterized by liquid dark excrements containing clots of undigested food; the faeces react alkaline and have a foul putrid smell. Microscopy of faeces reveals much fats, muscular fibres with vivid transverse and longitudinal striation and even ends (creatorrhoea). The content of organic compounds in the faeces is increased. The iodophilic flora is absent.
Diarrhoea occurring in organic affections of the large intestine is mostly of the inflammatory character. It is not copious, nor does it produce strong negative effect on the patient’s general condition (as compared with affections of the small intestine which is attended by profuse diarrhoea associated with deranged motor and absorption function of the intestine). The pronounced disorder in digestion causes some metabolic disorders in the patient (impaired absorption of proteins, iron, vitamins, and electrolytes).
Obstipation. This is obstinate constipation during which faeces are long retained in the intestine (for more than 48 hours). But the duration of constipation is only relative, because in many cases it is not the result of pathology but of the living conditions and nutrition. If vegetable food dominates in the diet, the subject may defaecate two or three times a day. Stools become rarer if the diet is rich in meat. A radical change iutrition can remove constipation. Limited mobility of the subject, hunger, and irregular defaecations (during the day) may prolong pauses between defaecation. The main factor determining defaecation is the condition of intestinal motor function. Bowel contents are retained in the large intestine and the rectum during constipation.
Organic and functional constipation is differentiated. Organic constipation is usually associated with mechanical obstruction, such as narrowing of the intestinal lumen due to a tumour, scar, adhesion, and also abnormalities in the intestine (megacolon, dolichosigmoid, megasigmoid, diverticulosis).
Functional constipation is subdivided into: (1) alimentary constipation; it occurs due to ingestion of easily assimilable foods, which leave small residue and normally stimulate peristalsis of the intestine by irritating its nervous receptors; (2) neurogenic constipation due to dysfunction of the intramural nervous apparatus or vagus nerve; these are the so-called dyskinetic constipation, caused by the reflex action on the intestinal motor function of another affected organ (cholecystitis, adnexitis, prostatitis, etc.), or by organic affections of the central nervous system (tumours of the brain, encephalitis, posterior spinal sclerosis); (.3) constipation associated with inflammatory affections, mainly of the large intestine (dysentery); (4) toxic constipation occurring in exogenous poisoning with lead, morphine, or cocaine; (5) constipation of endocrine aetiology, occurring in thyroid or pituitary hypofunction; (6) constipation caused by lack of physical exercise; (7) constipation caused by flaccidity of the prelum.
Intestinal haemorrhage often occurs in ulcerous affections of the alimentary system. It develops in the presence of tumour, protozoal and helminthic invasions, acute infections (typhoid fever, bacillary dysentery), in thrombosis of mesenteric vessels, ulcerous non-specific colitis, etc.
LIVER AND BILE DUCTS
Complaints. Patients with disorders of the hepatobiliary system usually complain of abdominal pain, dyspepsia, skin itching, jaundice, enlargement of the abdomen, and fever.
Pain is localized in the right hypochondrium and sometimes in the epigastrium and differs depending on the cause. Pain may be persistent and dull, or it may be severe and occur in attacks. Persistent pain is usually boring, or the patient feels pressure, heaviness, or distension in the right hypochondrium. Pain may radiate to the right shoulder, scapula, and in interscapular space (in chronic cholecystitis, perihepatitis and pericholecystitis, i.e. when the process extends onto the peritoneum overlying the liver and the gall bladder, and also in rapid and considerable enlargement of the liver which causes distension of Glisson’s capsule). This radiation of pain is quite characteristic of many diseases of the liver and gall bladder, because the right phrenic nerve, innervating the capsule in the region of the falciform and the coronary ligaments of the liver and the extrahepatic bile ducts, originates in the same segments of the spinal cord where the nerves of the neck and shoulder originate as well. Pain usually becomes more severe in deep breathing; in adhesion of the liver or the gall bladder to the neighbouring organs, pain is also intensified when the patient changes his posture, and sometimes during walking.
Attacks of pain (biliary or hepatic colics) develop suddenly and soon become quite severe and unbearable. The pain is first localized in the right hypochondrium but then spreads over the entire abdomen to radiate upwards, to the right, and posteriorly. An attack of pain may continue from several hours to a few days during which pain may subside and then intensify again; the attack ends as suddenly as it arises; or pain may lessen gradually. Attacks of pain occur mostly in cholelithiasis. They are provoked by jolting (as in riding) or by fatty food. Pain attacks occur also in hypermotoric dyskinesia of the gall bladder and bile ducts. Pain usually develops quite unexpectedly due to spastic contractions of muscles of the gall bladder and large bile ducts caused by irritation of their mucosa by a stone, and due to comparatively rapid distension of the gall bladder in congestion of bile (e.g. due to obstruction of the common bile duct by a stone). Warmth applied to the liver (provided the attack is not attended by considerable fever) and also administration of cholino- and myospasmolytics (atropine sulphate, papaverin hydrochloride, etc.) remove pain characteristic of the colic. An attack of hepatic colic can be attended by subfebrility (fever develops with pain and subsides with alleviation of pain), which is followed by a slight transient subicteric colour of the sclera or pronounced jaundice in obstruction of the common bile duct by a stone.
Pain developing in dyskinesia of the bile ducts is associated with upset coordination between contractions of the gall bladder and of the Oddi sphincter under the effect of increased tone of the vagus nerve. As a result, bile congests in the ducts, and the gall bladder is no longer emptied. This causes its convulsive contraction. Dyskinetic pain is characterized by the absence of signs of inflammation (leucocytosis, ESR, etc.).
Dyspeptic complaints include decreased appetite, often bitter taste in the mouth, eructation, nausea, vomiting, distension of the abdomen and rumbling, constipations or diarrhoea. These complaints are characteristic not only of diseases of the hepatobiliary system but also of other parts of the digestive system. Causes of these symptoms in diseases of the liver and bile ducts are explained by deranged secretion of bile (and hence impaired digestion of fats in the intestine) and derangement of the detoxicating function of the liver.
Fever occurs in acute inflammatory affection of the gall bladder and bile ducts, in abscess and cancer of the liver, in hepatitis, and active cirrhosis.
Skin itching attends hepatic or obstructive jaundice. It can develop without jaundice, as an early forerunner of the liver disease. Itching is caused by accumulation in the blood of bile acids which are otherwise excreted together with bile, or by stimulation of sensitive nerve endings in the skin. Itching is usually persistent and is a great annoyance to patients during night sleep (to cause insomnia). Severe itching causes scratching of the skin with its subsequent infection.
Icteric colouration of the skin and the visible mucosa (jaundice) is due to accumulation of bile pigments in the blood and tissues. Jaundice may develop unnoticeably to the patient and only the surrounding people may pay attention to the icteric colouration of the sclera and then the skin. In other cases jaundice can occur all of a sudden, following an attack of hepatic colics (in obstruction of the common bile duct by a stone in cholelithiasis). Jaundice may persist for months or even years, only slightly changing in intensity (chronic hepatitis and cirrhosis of the liver, benign bilirubinaemia). For details of the mechanism of developing jaundice and its diagnostic importance see below.
Enlargement of the abdomen (sometimes rapid) can be due to accumulation of ascitic fluid in the abdominal cavity (in obstructed blood outflow from the intestine via the portal vein), in considerable meteorism (due to deranged digestion in the intestine in upset bile excretory function), or in pronounced hepato- or splenomegaly. Vany chronic diseasemare attended by general wtacnes< non-motivated fatigue< and decreased work capacity.
PANCREAS
Pain, dyspepsia, jaundice, general weakness and wasting are the main complaints of patients with diseases of the pancreas.
Pain may vary in intensity and character. Attacks of paroxysmal pain, like in biliary colic, arising 3-4 hours after meals (especially after taking fatty food) are characteristic of calcareous pancreatitis. Pain is usually localized in the epigastrium or left hypochondrium to radiate into the back. Pain is sometimes so severe that can only be removed by spasmolytics co-evearcotics.
Pain is especially severe in acute pancreatitis. It develops suddenly and persists for a few hours or days and even weeks. The pain is usually localized in the upper abdomen and is often girdling in character. Severe pain and its vigorous onset in acute pancreatitis are explained by a sudden obstruction of the main pancreatic duct as a result of spasm and inflammatory oedema with subsequent sharp increase in pressure in small pancreatic ductules and irritation of the solar plexus.
Pain is very severe and prolonged in tumours of the pancreas. If the head of the pancreas is affected, pain is localized in the right hypochondrium and radiates into the back. If the tumour extends onto the body i tail of the pancreas, pain is felt in the entire epigastrium, left hypoclm drium, and its character may be girdling. Pain is intensified when the tient is in the recumbent position because the tumour presses on the so plexus. The patient would therefore assume a forced (half-bent) posture lessen the pain. Boring pain is characteristic of chronic pancrealiil although this form of the disease may be attended by severe pain as well.
Nausea and vomiting more frequently attend acute pancreatitis and are of reflex character. Chronic pancreatitis and tumour of the pancreas and are characterized by dyspepsia which is due to upset enzymatic activity ol il pancreas. Patients with chronic pancreatitis often complain of poor appetite, aversion to fatty foods, nausea, meteorism, diarrhoea with ample quid lustrous (fatty) and fetid faeces. Upset intestinal digestion can rapid cachexia and general weakness.
Cancer of the head of the pancreas is characterized by the following symptoms -Jaundice is of the obstructive type, progressive; the skin is dark-brown (with a greenish hue); there are severe itching, and haemorrhaesg. The tumour presses the terminal portion of the common bile duct to obstruct bile outflow. Jaundice may develop in sclerosis of the head of the pancreas as well. This is the result of chronic pancreatitis.
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General inspection
Mouth and throat. The major structure of the exterior of the mouth is the lips. The doctor should note the presence of painful, inflamed, and dried cracks or fissures of the lips, called cheilitis. These may be caused by exposure to harsh climatic conditions, habitual licking or biting of the lips, mouth breathing from respiratory distress, or dehydration, particularly with fever in systemic disease. Cheilosis, or angular stomatitis, is fissuring at the angles or comers of the lips and may indicate vitamin deficiencies of riboflavin or niacin.
Any lesions on the lips are noted. The herpes simplex virus produces singular or clusters of vesicular eruptions on the lip, which are often called “cold sores”. The lip may also be the site of a primary syphilitic chancre, which appears as a firm nodule that ulcerates and crusts. If one suspects a chancre, it is examined with a gloved hand for the doctor’s protection.
The doctor asks the patient to open his mouth wide, requests that he move his tongue in different directions for full visualization, and has him say “ahh” in order to depress the tongue for full view of the back of the mouth (tonsils, uvula, oropharynx). For a closer look at the buccal mucosa or lining of the cheeks, the doctor can ask the patient0 to use his fingers to move the outer lip and cheek to one side. The tongue blade is placed along the side of the tongue, not the center back area where the gag reflex is elicited.
All areas lined with mucous membranes (inside the lips and cheeks, gingiva, underside of tongue, palate, back of pharynx) are inspected, noting color, any areas of white patches or ulceration, bleeding, sensitivity, and moisture. The membranes should be bright pink, smooth, glistening, uniform, and moist. Any deviations are noted. For example, reddened areas with white ulcerated centers may be canker sores (aphthae), which may be caused by trauma to the gums during toothbrushing or chewing.
As the doctor observes the lining of the mouth, any odor (halitosis) is noted. Mouth odors are characteristic of a number of important health problems, such as poor dental hygiene, gingival disease, chronic constipation, dehydration, malnutrition, or systemic illness. A sudden, foul odor in the mouth may indicate a foreign body in the nose, particularly a bean or pea. The doctor should inspect the nose carefully and, if possible, remove the object with tweezers.
The teeth are inspected for number in each dental arch, hygiene, and occlusion or bite.. Discoloration of tooth enamel with obvious plaque (whitish coating on the surface of the teeth) is a sign of poor dental hygiene and indicates a need for dental counseling. Brown spots in the crevices of the crown of the tooth or between the teeth may be caries. Teeth that appear greenish black may be stained from oral ingestion of supplemental iron. Although unsightly, this disappears after the iron is no longer given.
Tooth Abscess: Tooth abscess involving left molar region. Associated inflammation of left face can clearly be seen.
Malocclusion or poor biting relationship of the teeth is evaluated in terms of (1) how the jaws relate to each other in vertical, transverse, and anteroposterior directions, for example, the “bucktoothed” appearance that results when the maxilla is forward in relation to the mandible, (2) how the teeth are aligned, and (3) how the teeth interdigitate when in occlusion.
The gums surrounding the teeth are examined. The color is normally coral pink, and the surface texture is stippled, similar to the appearance of orange peel. In dark-skinned individuals the gums are more deeply colored and a brownish area is often observed along the gum line.
The tongue is inspected for the presence of papillae, small projections that contain several taste buds each and give the tongue its characteristic rough appearance. Changes in the surface texture are noted, such as (1) “geographic tongue”, unusual patterns of papillae formation and denuded areas, (2) coated tongue, such as in thrush, or (3) an exceptionally beefy red and swollen tongue, which is a sign of various systemic diseases.
The doctor also notes the size and mobility of the tongue, especially protrusion, which is frequently seen in children with mental retardation. Normally the tip of the tongue should extend to the lips. If the patient is unable to move the tongue forward to this point, the frenulum, or central band of mucous membrane, which attaches the tongue to the floor of the mouth, may be too short. “Tongue-tie” can result in speech problems.
The roof of the mouth consists of the hard palate, near the front of the cavity, and the soft palate, toward the back of the pharynx, which has a small midline protrusion called the uvula. Both are carefully inspected to be sure that they are intact. Sometimes there is a pinpoint cleft in the soft palate, which may go undetected unless carefully inspected. Such a cleft is especially important if the uvula is bifid or separated into two appendages. A submucosal cleft may result in speech problems later on, since air cannot be effectively trapped for vocalization. The arch of the palate should be dome shaped. A narrow-flat roof or high-arched palate affects the placement of the tongue and can cause feeding and speech problems. Movement of the uvula is tested by eliciting a gag reflex. It moves upward to close off the nasopharynx from the oropharynx.
As the recesses of the oropharynx are inspected, the size and color of the palatine tonsils are also noted. They are normally the same color as the surrounding mucosa, glandular, rather than smooth in appearance, and barely visible over the edge of the palatoglossal arches. Enlargement, redness, and white patches on the tonsils and surrounding area are recorded. Such signs are indicative of suppurative tonsillitis or pharyngitis.
Left Peritonsilar Abscess. Note deveiation of uvula towards right.
The roof of the mouth consists of the hard palate, near the front of the cavity, and the soft palate, toward the back of the pharynx, which has a small midline protrusion called the uvula. Both are carefully inspected to be sure that they are intact. Sometimes there is a pinpoint cleft in the soft palate, which may go undetected unless carefully inspected. Such a cleft is especially important if the uvula is bifid or separated into two appendages. A submucosal cleft may result in speech problems later on, since air cannot be effectively trapped for vocalization. The arch of the palate should be dome shaped. A narrow-flat roof or high-arched palate affects the placement of the tongue and can cause feeding and speech problems. Movement of the uvula is tested by eliciting a gag reflex. It moves upward to close off the nasopharynx from the oropharynx.
As the recesses of the oropharynx are inspected, the size and color of the palatine tonsils are also noted. They are normally the same color as the surrounding mucosa, glandular, rather than smooth in appearance, and barely visible over the edge of the palatoglossal arches. Enlargement, redness, and white patches on the tonsils and surrounding area are recorded. Such signs are indicative of suppurative tonsillitis or pharyngitis.
